Diabetes lecture fall 2014

transcript

Caring for the Diabetic Client

N331 Health Maintenance & Restoration

∗ Total: 29.1 million children and adults in the United States—9.3 % of the population—have diabetes.

∗ Diagnosed: 21.0 million people

∗ Undiagnosed: 8.1 million people

∗ Prediabetes: 86 million people

∗ New Cases: 1.7 million new cases of diabetes are diagnosed in people aged 20 years and older in 2012.

American Diabetes Association National Diabetes Statistics Report, 2014

Diabetes Statistics

∗ 7.6% of non-Hispanic whites

∗ 9.0% of Asian Americans

∗ 12.8% of Hispanics

∗ 13.2% of non-Hispanic blacks

∗ 15.9% of American Indians/Alaskan Natives American Diabetes Association National Diabetes Statistics Report, 2014

Diabetes by Race/Ethnicity

∗ $245 billion: Total costs of diagnosed diabetes in the United States in 2012

∗ $176 billion for direct medical costs ∗ $69 billion in reduced productivity ∗ Average medical expenditures among people

with diagnosed diabetes were 2.3 times higher than what expenditures would be in the absence of diabetes.

American Diabetes Association National Diabetes Statistics Report, 2014

Cost of Diabetes

U.S. Diabetes Facts

NIDDK, National Diabetes Statistics fact sheet. HHS, NIH, 2011Source: 2005–2008 National Health and Nutrition Examination Survey

Age-Adjusted Prevalence of Obesity and Diagnosed Diabetes Among U.S. Adults Aged 18 Years or older

Obesity (BMI ≥30 kg/m 2)

Diabetes

No Data <14.0% 14.0-17.9% 18.0-21.9% 22.0-25.9% >26.0%

No Data <4.5% 4.5-5.9% 6.0-7.4% 7.5-8.9% >9.0%

CDC’s Division of Diabetes Translation. National Diabetes Surveillance System available at http://www.cdc.gov/diabetes/statistics

∗ Age∗ Ethnicity and family history∗ Body weight∗ Hypertension ∗ Dyslipidemia∗ Metabolic Syndrome∗ History gestational diabetes or delivered baby > 9 lb∗ Polycystic ovary syndrome∗ Prediabetes (Impaired glucose tolerance/Impaired fasting glucose)

Risk Factors

• Testing should be considered in all adults who are overweight (BMI ≥25 kg/m2*) and have additional risk factors:

• physical inactivity• first-degree relative with diabetes• high-risk race/ethnicity (e.g., African American, Latino, Native American, Asian American, Pacific Islander)• women who delivered a baby weighing >9 lb or were diagnosed with GDM• hypertension (≥140/90 mmHg or on therapy for hypertension)• HDL cholesterol level <35 mg/dl (0.90 mmol/l) and/or a triglyceride level >250 mg/dl (2.82 mmol/l)• women with polycystic ovarian syndrome (PCOS)• A1C ≥5.7%, IGT, or IFG on previous testing• other clinical conditions associated with insulin resistance (e.g., severe obesity, acanthosis nigricans)• history of CVD

______________________________________________________________________________________________

• In the absence of the above criteria, testing for diabetes should begin at age 45 years.______________________________________________________________________________________________

• If results are normal, testing should be repeated at least at 3-year intervals, with consideration of more frequent testing depending on initial results and risk status.

↵*At-risk BMI may be lower in some ethnic groups.

Criteria for testing for diabetes in asymptomatic adult individuals

Normal Physiology

Ingestion of meal

Increasedplasma glucose

Increased plasmaAmino acids

Insulin Secreted

Glycogensynthesis

Amino acid uptake+ protein synthesis

FFA + glycerolTransport +

TGL synthesis

Glucose uptake into muscle

cells & adipocytes

Normal Insulin Secretion

Fig. 49-1. Normal endogenous insulin secretion. In the first hour or two after meals, insulin concentrations riserapidly in blood and peak at about 1 hour. After meals, insulin concentrations promptly decline toward preprandial values as carbohydrate absorption from the gastrointestinal tract declines. After carbohydrate absorption from the gastrointestinal tract is complete and during the night, insulin concentrations are lowand fairly constant, with a slight increase at dawn.

Pathophysiology of Diabetes

Decreased insulinSupply/use

Glycogen catabolismIn liver & muscle

Protein catabolism&

gluconeogenesis

Fat catabolismFFA + glycerol

produced

Decreased transport of glucose into cellsCellular starvation

KetonesProduced by-product

of fat metabolism

CortisolEpinephrine

Growth hormone

Hyperglycemia

∗ Type 1 diabetes ∗ Type 2 diabetes ∗ Gestational diabetes∗ Prediabetes

∗ Impaired glucose tolerance∗ Impaired fasting glucose

Major Classifications

Pathophysiology

∗ Type 1:∗ Autoimmune

destruction of pancreatic beta cells thought to major cause.

∗ Leads to absolute insulin deficiency

∗ 5-10% of diabetics

∗ Type 2: ∗ Insulin resistance∗ Decreased insulin

receptors or inability to bind to muscle and adipose cells leading to inability to transport glucose into cell

∗ Defect in pancreatic beta cell secretion

∗ 90-95% of diabetics

Factors Contributing to Hyperglycemia

∗ Type 1: Acute onset∗ 3 P’s∗ Hyperglycemia, ketonuria∗ Weight loss, weakness, fatigue, dizziness

∗ Type 2: Onset may be slow ∗ Blurry vision, skin infections, vaginitis∗ Hyperglycemia∗ Target organ damage may already be present

Common Clinical Manifestations

Natural Progression of Type 2 Diabetes

-20 -10 0 10 20 30

Years of Diabetes

Relative β-Cell

Function

PlasmaGlucose

Insulin resistance

Insulin secretion

126 mg/dLFasting glucose

Postprandial glucose

Prior to diagnosis After diagnosis

Adapted from Bergenstal et al. 2000; International Diabetes Center.

The Changing Face of Diabetes

∗ Rapid rise of type 2 DM in minority populations.

∗ Increased rate of type 2 DM among children and adolescents.

∗ Increased recognition of type 1 DM in adults.

∗ Atypical forms.

Source: SEARCH for Diabetes in Youth StudyNHW=non-Hispanic whites; NHB=non-Hispanic blacks; H=Hispanics; API=Asians/Pacific Islanders; AI=American Indians

<10 years 10–19 years

Diagnosing Diabetes

Fasting Plasma Casual Plasma Oral Glucose A1C Glucose (FPG)* Glucose * Tolerance Test*

(Preferred Test) ________________________________________________________________________________________ Diabetes FPG >126 mg/dl Casual plasma Two-hour plasma > 6.5 %

glucose >200 mg/dl glucose (2hPG) >200 mg/dl

_______________________________________________________________________________________ Prediabetes Impaired Impaired Fasting Impaired Glucose 5.7-6.4 % Glucose Glucose (IFG)=FPG Tolerance (IGT) = Homeostasis 100 -125 mg/dl 2hPG >140 and

<199 mg/dl _______________________________________________________________________________________

Non-Diabetic FPG <100 mg/dl 2hPG <140 mg/dl < 6.5 %

*In the absence of unequivocal hyperglycemia, these need to be repeated on the second day

∗ Blood glucose – random, fasting, postprandial, capillary blood glucose

∗ Glucose tolerance test∗ HbgA1C or A1C∗ Glycosylated albumin∗ Ketonuria∗ Proteinuria:albuminuria, microalbuminuria∗ BUN, creatinine, GFR

Diagnostic Tests Used to Assess and Manage Diabetes

A patient screened for diabetes at a clinic has a fasting plasma glucose of 120 mg/dL (6.7 mmol/L). The nurse explains to the patient that this value:

1. Is diagnostic for diabetes. 2. Is normal, and diabetes is not a problem.3. Reflects impaired glucose tolerance, which is an early stage of diabetes. 4. Indicates an intermediate stage between normal glucose use and diabetes.

Knowledge Check…

A Constellation of Complications

GastropathyGastropathy

Autonomic Autonomic NeuropathyNeuropathy

Renal Renal DiseaseDisease

PeripheralPeripheral NeuropathyNeuropathy

Retinopathy/ Retinopathy/ Macular Macular

EdemaEdema

HypertensionHypertensionCardiovascular Cardiovascular

DiseaseDisease

DyslipidemiaDyslipidemia

Peripheral Peripheral

Vascular Vascular DiseaseDisease

Erectile Erectile DysfunctionDysfunction

DiabetesDiabetes

Treatment∗Glucose control∗Diet∗Exercise∗Weight loss – Bariatric surgery∗Diabetes medications – Oral, Insulin∗Blood pressure control – ACE inhibitors or ARB’s∗Blood lipid control – Statins ∗Preventive care practices for eyes, kidneys, feet, teeth and gums∗Aspirin as directed by physician

Preventing Diabetes Complications

NIDDK, National Diabetes Statistics fact sheet. HHS, NIH, 2005.

∗ Know therapeutic management plan∗ Assess client’s knowledge and self management

ability∗ Assessment and management of complications∗ Client education

Nursing Role

∗ Diabetes Control & Complications Trial (DCCT)∗ Compared intensive treatment to standard treatment in 1,441 people with type 1 diabetes∗ 60% reduction in risk between intensively treated group and standard group for retinopathy,

nephropathy, neuropathy (New England Journal of Medicine, 1993). ∗ Strict glucose control in type 1 diabetes reduces the risk of atherosclerosis (New England Journal of

Medicine, 2003).

∗ Hyperglycemia is an independent marker of in-hospital mortality in patients with undiagnosed diabetes (Guillermo et. al.,2002).

∗ Patients who are encouraged to become actively involved in managing their diabetes and feel they are competent to do so tend to be less depressed, more satisfied and have lower blood sugar levels (Williams et al., 2005).

∗ NICE-SUGAR study

Evidenced-Based Practice

∗ Plasma glucose (venous)∗ Capillary blood glucose – some meters

have a 15% difference between capillary and venous blood. Capillary blood glucose is lower.

∗ Continuous blood glucose monitoring – subcutaneous sensor

∗ Testing new non-invasive methods,eg.wristband.

Blood Glucose Monitoring

Goals for Glycemic Control

A1C* < 7.0%** Only 43% achieve goal

Pre- Prandial glucose

90-130 mg/dl

Postprandial plasma glucose

< 180 mg/dl

*For non-pregnant individuals ** goal for patients in general; <6% for individual patients if feasible/safe

Diabetes Care: Supp.1. 2011

Correlation of A1C with Average Glucose

A1C (%)Mean plasma

glucosemg/dl mmol/l

6 126 7.07 154 8.68 183 10.29 212 11.810 240 13.411 269 14.912 298 16.5

These estimates are based on ADAG data of ∼2,700 glucose measurements over 3 months per A1C measurement in 507 adults with type 1, type 2, and no diabetes. The correlation between A1C and average glucose was 0.92 (51). A calculator for converting A1C results into estimated average glucose (eAG), in either mg/dl or mmol/l, is available at http://professional.diabetes.org/eAG.

Management Principles for Older Adults with Complex Illness/Frailty

∗ Overall treatment goals need to be individualized

∗ Potential for hypoglycemic to occur from over aggressive treatment or from undesired adverse effects of medications or inadequate meal plans

∗ In the case of frail older adults, where the risk of hypoglycemia exceed benefit from tight control, the HgbA1c value can be used as a means of monitoring treatment without a target goal

*Used with permission from AACN GNEC Institute

6.5% to 7%HgbA1c levels

higher functioning older persons with diabetes

frail older adults with functional impairment and

limited life expectancy

∗ Critically ill patients:- glucose results 140-180 mg/dl- tighter control for some populations (CABG)

∗ Non-critically ill patients:- glucose results < 180 mg/dl

Diabetes Care 2011

Inpatient Glycemic Targets

ADA Recommendations: Hospital Care

∗ Identify in record as having DM and have order for blood glucose monitoring

∗ Sliding scale insulin NOT recommended∗ Hypoglycemia plan established and episodes racked∗ HbA1c drawn if none available form previous 2-3 months∗ Education plan and follow-up developed∗ New hyperglycemia - plans for follow-up testing documented∗ Assess: Pneumococcal and yearly influenza

Non-pharmacological Medical Therapy for

Type 2 Diabetes

Optimize BG Control Improve blood lipids Control blood pressure

Consistent carbohydrate intake

Monitor blood glucose to adjust therapy

Moderate weight loss –Bariatric surgery

Increase physical activity

Space meals

Modify fat and calorie content

∗ Improve glucose and lipid levels∗ Consistent day-to-day food intake.∗ Weight management.∗ Provide adequate nutrition across lifespan.

Nutritional Management: Goals

∗ CHO 40-60%∗ Protein 15-20% (reduced if client has renal disease)∗ Fat 30% or less

∗ Less than 7% saturated fat∗ No transfats

∗ Vitamin & mineral requirements are the same as general population.

Macronutrient Recommendations

∗ Carbohydrate counting∗ Calorie control diet, e.g.

∗ 1800 kcal ADA diet∗ Choose My Plate

Calories, Carbohydrates and Fat

∗ Fruits, vegetables, fruit juice∗ Breads, cereals, grains, pastries, starchy vegetables.∗ Milk and yogurt∗ If carbohydrate counting, 1 portion = 15 gm CHO∗ Typical meal = 4-5 portions (60-75 gm) CHO

∗ Carb counting activity∗ Breakfast 45g CHO∗ Lunch 60g CHO∗ Dinner 60g CHO

Example: Carbohydrate Counting

∗ Saturated (butter, hydrogenated fats)∗ Polyunsaturated (vegetable oil)∗ Monounsaturated- olive, canola∗ Transfatty acids – in processed foods, e.g. partially

hydrogenated . . ∗ Omega 3 fatty acids – cold water fish, walnuts

Focus on Type of Fat

∗ Benefits∗ Decreased blood glucose and improved insulin

sensitivity in type 2 diabetes∗ Improved lipids∗ Decreased blood pressure∗ Oxygen consumption increased∗ Improved blood flow∗ Reduced cardiovascular risks∗ Stress reduction∗ Weight control

Exercise Management

∗ Cardiovascular evaluation prior.∗ Eye exam to r/o risk for retinal detachment or

vitreous hemorrhage with exercise.∗ Assess for safety concerns related to

peripheral neuropathy.∗ Monitor CBG & B/P pre and post exercise.∗ Consistency

Exercise Readiness Assessment:

∗ Be knowledgeable regarding exercise plan.∗ Monitor for safety hazards.∗ Pre/post exercise assessment to monitor tolerance of

activity.∗ If BG < 100 snack prior;100-150 snack after; > 250 +

ketones, no exercise.

Nursing Role: Exercise

Management of Hyperglycemia with Pharmacologic Agents

Diabetic State

Where do hypoglycemic agents interact?

CHO Intake

Intestinal absorption

Decreased insulinsecretion

Increased hepaticglucose output Decreased peripheral

glucose uptake

Oral MedicationsClass Mechanism of Action

Sulfonylureasglipizide (Glucotrol), glyburide (Micronase, Diabeta) , glimepride (Amaryl)

Secretagogue: stimulates insulin secretion from beta cell

Meglitinidesrepaglinide (Prandin), nateglinide (Starlix)

Stimulate a rapid and short lived release of insulin from the pancreas

Biguanidemetformin (Glucophage), metformin ER (Glumetza)

Reduces hepatic glucose production; Sensitizer: increases insulin sensitivity to peripheral uptake, may cause lactic acidosis if kidneys are not functioning properly

Thiazolidineodionepioglitazone (Actos), rosiglitazone (Avandia)

Sensitizer: increases insulin sensitivity to peripheral uptake, causes edema, weight gain, not for heart failure pts.

a-glucosidase inhibitoracarbose (Precose), miglitol (Glyset)

Slows absorption of glucose, slows postprandial hyperglycemia

DPP-4 Inhibitorssitagliptin (Januvia), saxagliptin (Onglyza), linagliptin (Tradjenta)

Enhances the incretin system, stimulates release of insulin from pancreatic B cells.

SGLT2 InhibitorsCanagliflozin (Invokana)dapagliflozin (Farxiga)

Sodium-glucose transporter 2 (SGLT2) works in the kidney to reabsorb glucose, and this new class of medication, SGLT2 inhibitors, blocks this action, causing excess glucose to be eliminated in the urine. Prone to UTI

Therapeutic Agents for DiabetesClass Mechanism of ActionBile Acid Sequestrant (BAS) colesevelam (Welchol)

A cholesterol-lowering medication that also reduces blood glucose levels in patients with diabetes

Dopamine Receptor AgonistBromocitine (Cycloset)

Increases CNS dopamine receptor activity, increases insulin sensitivity and decreases A1C by improving postprandial hepatic glucose metabolism and increasing glucose uptake

IncretinsExenatide (Byetta)Exenatide ER once-weekly (Bydureon)Liraglutide (Victoza)

Stimulates release of insulin, decrease glucagon secretion, increase satiety, decrease gastric emptyingInjectable

Amylin AnalogPramlintide (Symlin)

Decrease gastric emptying, decrease glucagon secretions and endogenous glucose output from the liver, increase satiety. For type 1 diabetes.

∗ All patients with type 1 diabetes require insulin.

∗ Many patients with type 2 diabetes will eventually need insulin.

∗ As insulin deficiency progresses, a more physiologic multi-component insulin regimen will be required to adequately replace normal insulin secretion.

- Basal insulin - Meal-Related (prandial, bolus) insulin

Insulin Therapy in Diabetes

Insulins Onset Peak Duration Lispro* orAspart* ~15 minutes 60-90 minutes 2- 4 hours

Human Regular 30 – 60 minutes 2 – 3 hours 3- 6 hours

Human NPH 2 – 4 hours 4-10 hours 10-16 hours

Glargine* 1– 2 hours Peakless ~24 hours

*Insulin analogs

Insulin Action Comparison

Insulin Profiles

0 2 4 6 8 10 12 14 16 18 20 22 24

Regular (4-6 hours)

NPH (10-16 hours)

Glargine (~24 hours)

Aspart, lispro (2-4 hours)

Can you think like a pancreas ???

Basal / Bolus Concept

∗ The use of two insulins with different characteristics to mimic the pancreas.

∗ With the advent of long acting analogs insulin, we can mimic the pancreas by giving a slow release, virtually peakless, 24 hour basal insulin.

∗ Rapid acting analogs are preferred over Regular for meal or prandial dose to cover carbohydrates consumed at meals.

∗ The purpose of supplemental insulin (correction algorithm) is to bring a pre-meal elevated glucose level to target quickly and safely, used in addition to basal and bolus insulin.

∗ Blood sugars stay in target due to the basal/bolus insulins.

Review of Basal/Bolus Concept

∗ Basal insulins∗ Lantus (insulin glargine)∗ NPH

∗ Bolus insulins Correction scale / supplemental insulin /sliding scale∗ Humalog (lispro)∗ Novolog (insulin aspart)∗ Regular (best for tube feedings and hyperal)

∗ Premixed insulins∗ Humulin 70/30∗ Novolog 70/30 mix∗ Humalog 75/25 mix

∗ Special insulin∗ U 500

Insulin Therapy

∗ Lantus (glargine) daily, with a rapid-acting insulin immediately before meals.

∗ Supplemental insulin q4-6h with rapid-acting insulin

∗ Insulin + oral agents for type 2 diabetics e.g. ∗ BIDS – bedtime insulin, daytime oral medication

Insulin regimen examples:

Profiles of Human Insulins and Analogs

0 2 4 6 8 10 12 14 16 18 20 22 24

Glargine (~24 hours)

Aspart, lispro (2-4 hours)

Normal Insulin Secretion

Fig. 49-1. Normal endogenous insulin secretion. In the first hour or two after meals, insulin concentrations riserapidly in blood and peak at about 1 hour. After meals, insulin concentrations promptly decline toward preprandial values as carbohydrate absorption from the gastrointestinal tract declines. After carbohydrate absorption from the gastrointestinal tract is complete and during the night, insulin concentrations are lowand fairly constant, with a slight increase at dawn.

∗ Which insulin is the only one that can be given IV?

∗ Why might different routes be chosen?∗ Subc.∗ IV

Critical Thinking Questions…

∗ Syringes∗ 3/10cc = 30 units∗ 1/2cc = 50 units∗ 1cc = 100 units

∗ Insulin pens – prefilled or refillable∗ Needle-free technology: Jet injectors∗ Insulin pumps

Insulin Delivery Devices

Insulin Pump

Fig. 49-7. A, OmniPod Insulin Management System. The Pod holds and delivers insulin. B, The Personal DiabetesManager (PDM) wirelessly programs insulin delivery via the Pod. The PDM has a built-in glucose meter.

• Monitor CBG at appropriate times based on insulin dosing, meals and activity

• Assess for hyper and hypoglycemia at appropriate times: Know when insulins are peaking

• Insulin Storage:∗ Should be administered at room temperature.∗ Can keep a vial of insulin at room temperature for 28-30

days.∗ Avoid temperature extremes; maintain at 36-86 degrees F.∗ Unused,unopened vials should be stored in refrigerator

Steps to Successful Insulin Management

∗ Most serious:

∗ Side effects related to the injection:

∗ Other adverse effects:

∗ Lipodystrophy- happens when injections sites are not rotated

∗ Lipoatrophy∗ Lipohypertrophy

Side Effects

∗ Potential causes?∗ Didn’t eat enough∗ Skipped a meal

∗ Assessment of signs and symptoms∗ Mild to severe∗ Adrenergic symptoms∗ Neuroglycopenic symptoms∗ What class of drugs mask S/S?

∗ Management

Management of Hypoglycemia

Acute Complications - Hypoglycemia

Mild ∗ shaking∗ sweating∗ fast heartbeat∗ dizziness∗ hunger

Moderate Severe∗ impaired vision seizure∗ Headache unresponsive∗ Irritable coma

∗ Treatment mild-moderate hypoglycemia with 15 grams fast acting carbohydrate

∗ glucose tablets∗ glucose gel∗ 4 oz orange juice∗ 8 oz milk

∗ Test blood sugar in 15 minutes∗ Repeat treatment if needed

∗ Treat moderate-severe hypoglycemia or if NPO∗ Glucagon∗ D50

∗ Test blood sugar in 15 minutes∗ Repeat treatment if needed

Hypoglycemia - Treatment

∗ Somogyi effect

9 pm : Blood glucose 120 mg/dl8 am : blood glucose 210 mg/dl

∗ Dawn phenomena

Hyperglycemia Problems

Critical Thinking Questions…∗What are some possible causes of DKA?∗Assessment

∗ What might you expect the BG to be?∗ What fluid and electrolyte disturbances may result?∗ What might the pH and HCO3 be?∗ What clinical signs and symptoms may result?

Acute ComplicationsHyperglycemia: Diabetic Ketoacidosis

Diabetic Ketoacidosis

Fig. 49-11. Metabolic events leading to diabetic ketoacidosis and diabetic coma.

∗ Restore circulating blood volume∗ IV fluids

∗ Correct electrolyte imbalance∗ Potassium

∗ Normalize blood glucose∗ Insulin

∗ Correct acidosis

Goals of Treatment

Cardiac monitoring is initiated for a patient in diabetic ketoacidosis. The nurse recognizes that this measure is important to identify:

1. Dysrhythmias resulting from hypokalemia. 2. Fluid overload resulting from aggressive fluid replacement.3. The presence of hypovolemic shock related to osmotic diuresis.4. Cardiovascular collapse resulting from the effects of excess glucose on cardiac cells.

Critical Thinking Questions…∗Severe hyperglycemia without ketosis∗Who is at risk? ∗Assessment – what clinical manifestations may occur?

∗ Blood glucose level?∗ Acid/base balance?∗ VS∗ Other S/S?

Acute ComplicationsHyperosmolar Hyperglycemic Syndrome

(HHNS)

∗ Restore circulating blood volume∗ IV fluids

∗ Correct electrolyte balance∗ Potassium

∗ Normalize blood glucose∗ Insulin

Treatment Goals

∗ Blood glucose monitoring∗ CHO intake∗ Insulin needs∗ Ketone testing (Type I diabetes)

∗ When to notify healthcare personnel

∗ Prevention

Sick Day Management

A patient with type 1 diabetes calls the clinic with complaints of nausea, vomiting, and diarrhea. It is most important that the nurse advise the patient to:

1. Hold the regular dose of insulin.2. Drink cool fluids with high glucose content. 3. Check the blood glucose level every 2 to 4 hours.4. Use a less strenuous form of exercise than usual until the illness resolves.

Microvascular Complications

Hyperglycemia May Lead to Long-Term Complications in Multiple Organs

Neuropathy

CerebrovascularDisease

PeripheralVascular Disease

Macrovascular Complications

Retinopathy

12 % of all new cases of blindness

Nephropathy

>40% new cases ESRD

Heart Disease

Diabetes Control and Complications Trial Research Group. N Engl J Med. 1993;329:977-986.Stratton IM et al. BMJ. 2000;321:405-412 with permission from the BMJ Publishing Groupwww.cdc.gov.

Diagnosed in 37.2% patientswith diabetes > 35 years old

60-70% have mild to severe nervous system damage

Chronic Complications

∗ Microvascular∗ Retinopathy∗ Nephropathy∗ Neuropathy

∗ Macrovascular∗ Accelerated large vessel

cardiovascular disease (PVD, CAD, CVA)

∗ Autonomic Neuropathy∗ Fixed heart rate∗ Orthostatic hypotension∗ Delayed gastric emptying∗ Urinary retention∗ Impotence

Nursing Management: Retinopathy

Retinopathy :•Encourage regular eye exams•Vision aids•Safety precautions

Nursing Management Nephropathy: Impaired urinary elimination; Risk FVE

∗ Monitor:∗ Intake/output∗ Serum electrolytes∗ Bun, creatinine, GFR∗ Lung sounds, o2 sats, edema

∗ Monitor need to adjust drug dosages based on renal clearance

Nursing Management Retinopathy and Neuropathy: Disturbed sensory perception

∗ Neuropathy:∗ Foot care∗ Fall prevention for postural

hypotension∗ Prevention of aspiration,

attention to hyper/hypoglycemia with gastroparesis

∗ Prevention of urinary retention

∗ Monitor for fixed heart rate with activity

Acceleration of Macrovascular Disease

∗ Peripheral vascular disease

∗ Cerebrovascular disease∗ Atherosclerotic heart

disease∗ Cardiomyopathy∗ Hypertension

The risk for development of coronary artery disease is 2- to 4-fold greater and the risk of cardiac events of a lethal nature subsequently higher when diabetes is present. Insulin resistance even without diabetes increases coronary risk.

Diabetes & Heart Disease

∗ Daily foot care and inspection∗ Always wear protective shoes/slippers∗ Wear good-fitting shoes∗ Cotton socks vs nylon socks∗ Avoid home remedies for corns,

calluses, ingrown toenails∗ Cut nail straight across∗ Avoid temperature extremes∗ Seek immediate medical attention for

any injury or problem

Foot Care

Impact of Comorbidities

∗ Older adults, over age 65 and in particular, those of advanced old age, typically experience ∗ Multiple comorbidities∗ Higher rates of physical disabilities functional impairment∗ Geriatric syndromes

∗ Depression∗ Cognitive impairment∗ Falls ∗ Urinary incontinence

Gerontologic Considerations

∗ Prevalence increases with age.∗ Presence of delayed psychomotor function could

interfere with treating hypoglycemia.∗ Must consider patient’s own desire for treatment and

coexisting medical problems ∗ Recognize limitations in physical activity, manual

dexterity, and visual acuity∗ Education based on individual’s needs, using slower

Impact of Geriatric Syndromes

∗ These syndromes are included in current screening recommendations for older adults with a diagnosis of Type 2 Diabetes

∗ Further screening for these events within three to six months of a new diagnosis should accompany the initial evaluation period

Cognitive impairmentDepressionPoly-

pharmacyGeriatric

SyndromesPersistent

painInjurious fall Urinary incontinence

Atypical Presentation of Clinical Conditions in Older Adults with

Type 2 Diabetes Integument Skin infections (examples include non-healing venous stasis

ulcers; non-healing traumatic wounds)

Cardiovascular Chest pain (examples include acute coronary syndromes; de novo cardiac ischemia) 1

Neurological

Altered level of consciousness with non- focal neurological signs (examples include stupor associated with no focal neurological deficits and hyperglycemic, hyperosmolar, non-ketotic coma) Paresthesia of distal extremities (diabetic peripheral neuropathy) 1

Gento-urinary Erectile dysfunction; Vaginitis*Used with permission from AACN GNEC Institute

Urinary Incontinence ∗ Older women with Type 2 Diabetes at increased risk for

urinary incontinence due to chronic hyperglycemia∗ Physiologically, excess glucose in the serum causes

hyperosmolarity and shifts in fluid balance∗ Chronic hyperglycemia directly effects the genito-urinary

system by causing symptoms of frequency, polyuria, nocturia and potentially urinary incontinence

∗ Screen: Urinary incontinence at history taking and review of systems during the initial evaluation of the older adult with Type 2 Diabetes

∗ Altered health maintenance∗ Knowledge deficit∗ Imbalanced nutrition∗ Fluid volume deficit∗ Impaired tissue perfusion∗ Risk for injury∗ Disturbed sensory perception∗ Spiritual distress

Nursing Diagnoses

Self-Management Education∗ Older adults with diabetes have special educational needs

secondary to sensory and other deficits related to the aging process

∗ Educational plan:∗ Include an assessment of the individual’s priorities∗ Use easily read or heard messages and proceed at a slower

pace utilizing significant others and caregivers in instruction

∗ Elderly persons with diabetes need assistance with organization of information so they can slowly adapt it to their activities of daily living

Ideally, the goal of patient diabetes education is to:

1. Make all patients responsible for the management of their disease.

2. Involve the patient’s family and significant others in the care of the patient.

3. Enable the patient to become the most active participant in the management of the diabetes.

4. Provide the patient with as much information as soon as possible to prevent complications of diabetes.

Case Study∗ 52-year-old woman was diagnosed with type 2 diabetes 6 years ago.∗ Did not follow up with recommendations for care∗ She works as a banking executive and gets little exercise.∗ She has gained 18 pounds over the past year and eats a high-fat diet. ∗ Complaining of weakness in her right foot

∗ Began 1 month ago ∗ Difficult to dorsiflex and feels numb

∗ Also complains of an itching rash in her groin area∗ Has had rash on and off for many years∗ Worse when weather is warm

∗ Increased thirst and frequent nighttime urination∗ Denies other weakness, numbness, changes in vision∗ BP 162/98

Case Study

∗ Random glucose test 253 mg/dL∗ Hb A1C 9.1%∗ Urine dipstick positive for glucose and negative for

protein∗ Wet prep of smear from rash consistent with Candida

albicans∗ ECG with evidence of early ventricular hypertrophy by

voltage

Discussion Questions

1. She wants to know why all of these changes have been happening to her body. How would you explain this to her?

2. What is the priority nursing intervention?3. What teaching should be done with her?

Diabetes lecture fall 2014

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