Chapter 47 Osborn & Wraa: Caring for Patients with DiabetesI. Diabetes Mellitus

A. Group of metabolic disorders characterized by abnormal fuel metabolism, all of which have hyperglycemia in common.

B. Prevalence of diabetes differs by type of diabetes, race, ethnicity, and geographic location

C. American Diabetes Association ADA have the most recent criteria for diagnosis and classification with periodic updates

II. Types of Diabetes A. Type 1 Diabetes Mellitus

Lacks insulin production caused by autoimmune destruction of insulin-producing pancreatic beta cells i. Epidemiology and Etiology

o Frequently diagnosed BEFORE age 30 o Latent autoimmune diabetes in adults LADAo 5-10% of all diagnosed diabetes o Thin, normal weight, abrupt symptom onseto Results from genetics, environment and autoimmunity o Risk Factors for Type 1:

1. Genetics Familial predisposition High chance from father (6%) compared to mom (3%)

and monozygotic twins (25-50%) compared to dizygotic twins (6%)

2. Environmental Viral infections, dietary factors, toxins (N-nitroso

compounds), congenital rubella syndrome, cow’s milk proteins,

3. Autoimmunity Circulating autoantibodies that target pancreatic beta-cell

components: ICAs, IAAs, GAD Presence of 2 or more antibodies, together with alterations

in insulin secretion is predictive of type 1 diabetes development

B. Type 2 Diabetes Mellitus Decreased insulin production by pancreas Increased insulin resistance

i. Epidemiology and Etiology o Diagnosed AFTER age 30 o 90-95% of all diabetes o Overweight, obese, strong family hx of disorder o Insulin therapy and/or oral medications for hyperglycemia o Risk factors for type 2 diabetes:

1. Sedentary Lifestyle and Poor Dietary Patterns Finnish Diabetes Prevention Study: reduced (weight,

dietary fat and saturated fat) + increased (dietary fiber and physical activity)= reduced diabetes risk 58%

US Diabetes Prevention Program: lifestyle modification program prevalent over metformin medication

High carb, high fat, high alcohol and low fat diets contribute to development of type 2

2. Ethnicity Wide variability in risk of type 1 among racial and ethnic

groups3. Obesity

Central obesity: glucose intolerance, hyperinsulinemia, hypertriglyceridemia.

Bisceral obesity: weight centered in abdomen 4. Metabolic Syndrome

Group of metabolic abnormalities that predispose individuals to CVD and type 2

Abnormalities: insulin resisteance, glucose intolerance, hyperinsulinemia, hypertriglercidemia, and decreased HDL cholesterol, central obesity and HTN.

Aka insulin resistance syndrome. Can develop into type 2. Prevention through weight loss, diet, & exercise

C. Risk Factors For Type 2 Diabetesi. Age, sedentary lifestyle, poor dietary habits, obesity, intrauterine

development, familial history, ethnicity, metabolic syndrome, gestational diabetes, prediabetes, high blood pressure, polycystic ovary syndrome (PCOS), HX of previously impaired glucose tolerance, presence of acanthosis nigicans, history of cardiovascular disease, drug induced diabetes, endocrine disorders, genetic diseases, urbanization and soceioeconomic status. On page 1420

D. Gestational Diabetes Mellitus Diabetes onset during pregnancy 2-10% for all pregnancies Risk factors: previous GDM, advanced maternal age, oesity, family hx of

diabetes and racial ethnic origin (American: African, Hispanic Latino, Indian) Treatment: diet, oral meds, insulin therapy for hyperglycemia Uncontrolled hyperglycemia= fetal/ maternal complications

E. Other Specific Types of Diabetesi. Monogenic Diabetes

1. Epidemiology, Etiology and Risk Factors 1-5% of all childhood diabetes From single-gene mutation (type 1,2 is from mult) Neonatal diabetes mellitus= newborn, infant Maturity-onset diabetes of young= adolescence, early adult Medical Management: MODY treated with oral diabetes

meds ii. Latent Autoimmune Diabetes in Adultso Genetically linked, hereditary autoimmune disease. 1.5 diabetes o Perceives pancreas as foreign and kills insulin-producing beta cellso Common AFTER age 30 o Risk factors: age, acute symptoms of diabetes, BI <35 kg/m, personal

hx of autoimmune disease 1. Clinical Manifestations and Pathophysiology

Symptoms: age (30-50), lean build, normal-low BMI, no ketoacidosis, no known type 2 relatives, low C peptide level

Requires insulin within 3 years at point of diagnosis LADA pt has less autoantibodies than type 1

2. Medical Management No single optimal treatment. Must distinguish LADA pt from

type 2 so drugs are not mistaken Control hyperglycemia Reduced calorie diet, increase physical activity, oral

antidiabetic meds. Similar diet to type 1 iii. Secondary Diabetes

1. Pancreas’s inability to produce sufficient amounts of insulin BUT is a reaction to other internal diseases or conditions

2. Epidemiology, Etiology, and Pathophysiology NIDDK: 1-5% of diabetic cases Caused by damage, injury, destroyed pancreas;

medications; body’s rxn to surgery involving pancreas 3. Clinical Manifestations, Lab Tests and Medical Management

Same manifestations to primary diabetes. Treated like type 2 or destructs insulin making beta cells,

resemble tpe 1 treatment and insulin injections iv. Prediabetes

1. People with glucose intolerance and at increased risk for developing diabetes

2. Impaired fasting glucose: fasting blood glucose or HG A1c is higher than normal

3. Impaired glucose tolerance: blood glucose level 2 hours following oral glucose is higher than normal nut not diagnostic of diabetes

4. Increased risk of CVD, stroke, diabetes.5. Normalize with diet modification, weight loss, physical activity

III. Physiology of Fuel MetabolismA. Pathophysiology of Type 1 DiabetesB. Pathophysiology of Type 2 Diabetes

IV. Clinical Manifestations of Type 1 and Type 2 Diabetes A. Signs and Symptoms of diabetes without metabolic complications (DKA, HHS)

i. Glucosuria, osmotic diuresis, polyuria, nocturia, hypotension, tachycardia, polydipsia, polyphagia, weight loss, fatigue

B. Complications of Diabetesi. Retinopathy, glaucoma, loss of sensation in foot, skin dryness, cracjing,

callus, infections, itching, dermopathy, blisters, poor wound healing, hearing loss, problems with teeth, gums heart disease, PAD, HTN, stroke, gastroparesis, neurogenic bladder, diabetic diarrhea, kidney disease, ketoacidosis, HHNS, neuropathy, charcot deformity, lower extremity ulceration, sexual dysfunction

V. Laboratory Tests and Diagnostic ProceduresA. Blood Glucose Levels

i. Measured following overnight fast – no food or drink with exception of water for 10-12 hours

ii. Used for diagnosis of prediabetes and diabetesB. Oral Glucose Tolerance Tests

i. Confirms diagnosis of diabetes ii. Fast 10 hours prior and intake carbs 150 g/day for 3 days prior iii. Refrain from smoking during test (time between blood draws)

C. Self-Monitoring of Blood Glucose i. Pt instructed to perform preprandial blood glucose measurements

(immediately prior to meal and snack) postprandial blood glucose measurement (approx. 2 hours after meal or snack) or when experiencing symptoms (hypoglycemia)

ii. Steps:1. Strips must be current, properly stored and appropriate

temperature 2. Calibrate to correct lot number3. Meter must be clean4. Adequate blood amount on strip5. Fingertip should be clean and dry pior to puncture

iii. Safety Alert: Hospitalized pt eating 4x a da should perform blood glucose before each meal or snack. Calculation prebreakfast dose of rapid acting insulin should be based on glucose made shortly before breakfast (not hours prior). T not eating also should have glucose levels checked 4x a day or every 6 hours depending on insulin regimen

D. Continuous Blood Glucose Monitoring i. Medtronic measures glucose levels in interstitial fluid every 10 seconds

and provides average blood glucose level every 5 minutes. Sensor is small with tubing and small cannula inserted into subcutaneous tissue (abdomen) and results transmit ti insulin pump and read in real time and stored to be downloaded. Pt and health care provider discuss trends on bg patterns and treatment decisions

E. Hemoglobin A1C Testi. Primary lab test to monitor long term glucose control. Formed when blood

glucose binds irreversibly to hemoglobinF. Urinary Glucose

i. Self-monitoring blood glucose replaced this G. Urinary and Blood Ketones

i. For diabetes self management (type 1), pregnancy with preexisting diabetes and gestational diabetes.

ii. Type 1 should test urine for ketones during stress or infection, when blood glucose are elvated >300 and DKA symptoms ab pain, n/v.

iii. Bedside and self testing kits too H. Diabetes Diagnosis

i. National Guidelines for Establishing a Diagnosis of Diabetes:1. HgA1C 6.5% or higher. 2. C-peptide negative (no insulin)3. Urine test has glucose and ketones

I. Prediabetes Diagnosis i. Impaired blood glucose tolerance and often occurs together with

metabolic syndrome but not alwaysii. Impaired glucose tolerance= 2 hour plasma blood glucose level <140

and <200 mg/dL following 75 g oral glucose J. National Guidelines for Establishing a Diagnosis of Diabetes

i. American Diabetes Associate (ADA)

1. Fasting blood sugar > 126 mg/dL on more than one occasion with or without hyperglycemia symptoms

2. Casual serum blood glucose >200mg/dL along with hyperglycemia symptoms (polydipsia, polyuria)

3. 2 hour oral glucose tolerance test of >200mg/dL VI. Medical Management

o Type 1 (insulin replacement), Type 2 (oral med, insulin), Anti-htn, lipid-lowering drugs, exercise, good nutrition, lifestyle change A. Goals of Diabetes Management

i. Long term: prevent long term complicationsii. Short term: prevent severe hypoglycemia, hyperglycemia, DKA, and

HHSiii. From the DCCT and UKPDS studies, glycemic control is emphasized to

manage diabetes, and reduce CVD but did not reach statistical significant.

1. Glycemic goal: A1C <7%, Preprandial blood glucose 90-130 mg/dL, Postprandial blood glucose <180, blood pressure <130/80, Lipid goal: LFL<100, Trigylceride<150, HDL >40

2. Lifestyle changes (exercise, stop smoke, diet, medication ) B. Management of Type 1 Diabetes

o Primary tx: Insulin replacement therapy (injection or pump) i. Insulin Preparations

Characterized by onset, peaks and duration of action Insulin secretion is basal or meal stimulated Commercial insulin preparations are rapid, short, intermediate and

long acting 1. Rapid Acting Insulin

Onset: 15 minutes; Peak: 1-2 hours; Duration 3-4 hours Before meal or snack, OR after meal. Safety Alert: Should be injected as close to meal or nack

as soon as possible to avoid hypoglycemia. Nurse role is to be alert for S&S of hypoglycemia and educate about how to prevent/treat hypoglycemic rxn

2. Short Acting Insulin Onset 15 min-1 hour; Peak: 1-5 hours, Duration 6-10 hours Regular insulin injected 30-45 minutes before meals Regular insulin replaced by rapid-acting insulin analog

3. Intermediate Acting Insulin Onset: 1-2 hours; Peak 6-14 hours, Duration 16-24 hours NPH insulin, provides basal insulin (2 injections a day) Limit NPH because high plasma during peak increases

hypoglycemia risk 4. Long-Acting Insulin

Onset 1 hour, Peakless, Duration 24 Basal insulin coverage and small peak

5. Premixed Insulins Combination of rapid or short acting insulin preparations

mixed with inetermediate acting insulin. Ex. 70%NPH and 30% regular insulin

Not easy to adjust premeal and basal insulin 6. Incretin Mimetics

Injectable meds used adjunctive to mealtime therapy to improve glycemic control in type 2.

Incretin mimetics enhance glucose dependent insulin secretion from pancreatic beta cells which reducing postprandial glucose levels

Side effect: nausea Decrease rate of oral medications so administer them

1 hour before injection of mimetics. 7. Amylin Analog

Reduces postprandial blood by slowing gastric emptying, suppress glucagon, promote satiety,.

Inject SQ immediately before meal for type 2 glycemic control. Mealtime therapy for type 1

Administer other medications1 hour before or 2 hours after administering pramlintide (amylin analog) because it affects GI motility

ii. Insulin Delivery Devices1. Continuous subcutaneous insulin infusion CSII –intensive insulin

therapy via pump. Pump made out of a pump reservoir (syringe) filled with insulin, small battery operated pump, and a computer chip. Reservoir connects with tubing with a needle or cannula through which insulin is delivered. Cannula inserted SQ in abdomen.

2. Pump delivers 24 hours a day programmed rate specific to patient 3. Designed to mimic basal and meal stimulated patterns 4. Program to infuse differing basal rates thru 24 hour period

iii. Insulin Regimes Type 1 insulin therapy goal is to normalize blood glucose levels which

is done by using combinations of insulin 1. Twice-Daily Injection Regimen

Regular or rapid acting insulin combines with intermediate (NPH)

Prior to breakfast and prior to supper Gives little flexibility to changing mealtime and NPH peak

predisposes hypoglycemia if skipping a meal 2. Three-Times Daily Insulin Injection Regimen

Regular or rapid acting insulin combines with NPH Prior to breakfast, regular or rapid acting insulin prior to

dinner and NPH prior to bedtime Difference from twice is that it is at bedtime Two causes

i. Dawn phenomenon- fasting hyperglycemia without prior nocturnal hypoglycemia. Occurs when growth hormone is secreted at night. Pt awake with elevated fast blood glucose. Pregnant women is more exaggerated due to excessive hormones at night. 

ii. Somogyi effect- fasting hyperglycemia with prior hypoglycemia. Aka rebound hyperglycemia. Pattern of undetected hypoglycemia followed by hyperglycemia. Happens at night or when too much insulin. 

iii. To differentiate between somgyi or dawn, test blood glucose at night. Hypoglycemia at night then somogyi effect. Hypoglycemia not present at night then dawn. 

3. Four-Times Daily Insulin Regimen NPH and rapid or short acting insulin at breakfast time,

rapid or short acting insulin before lunch and dinner and just NPH at bedtime. Premeal insulin helps reduce postprandial hypoglycemia. NPH provides basal insulin

4. Other Insulin Regimens Peakless insulins provide better basal insulin coverage. Multiple-dose regimen: long acting insulin is used in

combination with rapid acting insulin prior to each meal. Insulin pump- mimics normal insulin secretion because it is

programmed VII. Nursing Management

o 1) Instruct pt in prescribed insulin delivery (pen, syringe, pump)o 2) Review Insulin delivery techniques o 3) Instruct on specific insulin regimen and assess understanding o 4) instruct on relationship between glucose monitoring and regimeno 5)help them understand how prescribed adjustments in insulin affects

glycemic controlo 6)help them understand S&S hypo and hyperglycemia

A. Management of Type 2 Diabetes i. Oral Diabetes Medications

1. Sulfonylureas Treats type 2 Stimulates insulin from pancreatic beta cells Side effect: hypoglycemia, allergy to sulfa; alcohol causes

warmth, flush, headache, n/v, sweat, thirst 2. Meglitinides

Treats type 2 to reduce hyperglycemia with nutrition and exercise

Rapid insulin secretion from pancreatic beta cells Give prior to each meal to reduce postprandial

hyperglycemia Side effect: hypoglycemia. Eat within 20 minutes of medication to prevent

hypoglycemia3. Alpha-Glucosidase Inhibitors

Will reduce postprandial glucose levels since postprandial hyperglycemia contributes to diabetes

GI effects: softer stools, diarrhea, flatulence and bloating. These can be reduced by titrating slowly up

Hypoglycemia can occur so pt must use pure glucose: fruit, juices, glucose tablets to treat and because carb absorption is delayed

4. Biguanides Reduces hepatic glycogenolysis and glucogenolysis

results in decreased hepatic glucose and low blood glucose.

GI effects: n/v/d, and can be prevented by slow titration. Screen pt who are great risk of lactic acidosis since this is

a lifethreatening adverse rxn 5. Thiazolidinediones6. Dipeptidyl Peptidase-4Inhibitors 7. Combinations of Oral Medications

When a pt fails oral monotherapy, combining drugs of different classes is usually more effective than stopping one and substituting another.

When pt requires near-max dose of one med, adding another drug is usually better than increasing dosage of original medication

Secondary failure of two-drug combo in pt wth type 2 is expected eventually.

Three-drug combo is useful but adding insulin to existing regimen or insulin alone should be sufficient

ii. Insulin Therapy for Type 2 Diabetes 1. Supplements reduction of insulin secretion and overcomes insulin

resistance 2. Start off with oral meds but then require insulin treatment for

glucose control 3. Insulin in combination with oral medication to suppress hepatic

glucose production during the night. (oral meds during day) VIII. Nursing Management

i. For oral hypoglycemic therapy is 1. Instruct pt in prescribed oral hypoglycemic meds2. Review oral hypoglycemic therapy with pt who have been on it

prior to visit3. Instruction pt on relationship between glucose monitoring and oral

hypoglycemic medications4. Help pt understand how prescribed adjustments in oral meds may

affect glycemic control5. Understand S&S of hypoglycemia and hyperglycemia

IX. Nutrition and Diabetes i. Nutrition and physical activity ii. MNT – medical nutrition therapy- meal planning approaches

B. Micronutrients and Macronutrients in the Diet i. ADA recommendations for prediabetes, diabetes and diabetes

complications C. Medical Nutrition Therapy

i. No “single” diabetes dietii. Mealplanning can be flexible or not (traditional insulin regimen)iii. ADA Exchange List- foods categorized into groups- bread/starch eat,

fruit, veggies, fats) and assigned specific amount based on daily calories

iv. Pt instructed to read food labels to determine total amount of CHO in a food item

D. Nutritional Needs of Hospitalized Patients i. Caloric need met through provision of 25 to 35 kcal/kg body weight ii. Oral route of feeding is preferred. If not, then enteral and parenteral

feeding

iii. CHO counting is integrated into the diet of the hospital pt in various ways

X. Exercise and Physical Activity i. Benefits for those already with type 1 and type 2: low blood glucose

levels, improved insulin sensitivity, improvements in cardiovascular risks (high lipid and BP levels, improved cardiac conditioning, increased strength, flexibily, personal well being)

ii. Best used with calorie restricted diet iii. Fuel mobilization from muscle and liver stores during exercise in

individuals with diabetes during exercise may be 20 fold higher than that during sedentary activity to maintain normal blood glucose. Plasma insulin decrease while regulatory hormones increase to maintain glucose homeostasis

iv. Safety Alert: Pt with diabetes using pharmacologic therapy are at greater risk for hypoglycemia during the following exercise. Hypoglcemic effect can persist for several hours and pt education about preventing and treating exercise related hypoglycemia is essential**

v. Diabetes individuals can participate in all levels of physical activity. Metabolic response varies depending on plasma glucose levels at time of exercise. Poor metabolic control is at risk for worsening hyperglycemia nd ketosis

vi. In type 2, regular exercise plays a key role in improving long term metabolic control positive impact on insulin resistance

vii. Guidelines for exercise:1. Avoid exercise when blood glucose is > 250 mg/dL and ketones

present, caution if blood glucose is >300 mg/dL w/o ketosis2. If bloog glucose is <100 prior to exercise, ingest CHO food 3. Monitor blood glucose before, after and more frequently during

postexercise period 4. Self monitor blood glucose in response to different activities5. Maintain CHO foods readily available after exercise

B. Exercise and Diabetes Complicationsi. ADA recommends a detailed medical evaluation with appropriate

diagnostic studies prior to beginning an exercise program1. Graded exercise test, pre-exercise assessment- evaluates for

PVD, retinal exam, evaluates renal fxn, assess autonomic and peripheral neuropathy.

2. Complications will not disallow participation of exercise but requires medical team attention

C. Exercise Prescriptions i. Individualized with emphasis on enjoyment ii. 5-10 min warm up, 5-10 minutes of gentle stretching, a period of aerobic

activity, and 5-10 minutes of cool down. iii. Type 2 should have minimum of 150 minutes per week of exercise

(moderate or higher)iv. Aerobic activities- 10 minute intervals spread throughout week

XI. Health PromotionA. Nurse’s role is the primary prevention of type 2 and secondary prevention of the

complications of type 1 and 2 B. Nurse develops individualized programs to reduce risk of type 2 by assessment

of pt and family who are obese/overweight

C. Nurse helps both type 1 and type 2 with lifestyle and physical activity changes D. Complementary and alternative medicine CAM

i. Example: prayer, acupuncture, massage, biofeedback, yoga, plant remedies

ii. Nurse must understand that nonpharmalogic meds are supplemental therapy

XII. Management of Hospitalized Patients with Diabetes i. Infection and stress of illness/surgery worsens glycemic control in

diabetic pt and precipitates hyperglycemia B. Hyperglycemia in Acute Illness

i. Hyperglycemia results from stress from illness/ surgery, and increase insulin resistance

ii. Hyperglycemia interferes with infection recovery and wound healing C. Target Glucose Levels for Hospitalized Patients

i. Target glucose levels vary for critically ill and non critically ill pt ii. Critically ill pt: insulin therapy for hyperglycemia- no greater than

180mg/dLiii. Non-critically ill pt: no clear evidence for specific blood glucose goals.

Blood glucose should be 140-180 mg/dLiv. Non-critically ill: schedules SQ insulin injections with basal, nutritional

and supplemental insulin correction doses D. Insulin Protocols Designed to Meet Treatment Goals in Hospitalized Patients

i. Evidence supports IV insulin infusions in ICU for hyperglycemic critically ill

ii. Protocol to infuse glucose to prevent hypoglycemia iii. Insulin infusions are effective with NPO, parenteral nutrition and enteral

tube feedings. Allows for greater flexibility in changing insulin dosage and preventing hypoglycemia

iv. Can transition from IB infusion to SQ insulin. v. Oremeal insulin, basal insulin dose and correction factor. Correction

factor is an additional amount of insulin provided with each meal based on the premeal blood glucose.

E. Diabetic Ketoacidosisi. Life threatening complication precipitated by acute or deficiency in

insulin secretion. ii. Characteristics: disturbance in metabolism of CHO, fat and protein iii. Treated in ICUiv. Pt care: severe dehydration, insulin deficiency, metabolic acidosis from

ketosis and lactic acidosis, depletion of electrolytes from osmotic diuresis,

F. Hyperosmolar Hyperglycemic Syndromei. life threatening complication characterized by serum hyperosmolarity,

dehydration and hyperglycemia ii. Cannot recognize thirst or express need for water iii. Excessive unreplaced fluid losses, secondary to massiv glycosuric

diuresis, following gi fluid losses and limited fluid intake G. Hypoglycemia

i. Hypoglycemia Unawareness 1. Loss of autonomic nervous system responses to low blood

glucose

2. Symptoms: tachycardia, sweating, palpitations prompts pt to eat to prevent hypoglycemia but unawareness is results deficient glucagon and epinephrine response to hypoglycemia

XIII. Chronic Complications of Diabetes and Associated Medical Treatment A. Diseases of the Heart and Blood Vessels

i. Coronary heart disease, PBD and stroke ii. Diabetics with heart disease are at risk for death 2 times more than

those without diabetes iii. Risk for stroke is higher in diabetic pt

B. Kidney Diseasei. Diabetes is the leading cause of chronic kidney disease ii. Diabetic nephropathy- asymptomatic and detected from routine lab

tests. Increased GFR, to ESRD characterized by proteinuria, decreasing GFR and increasing creatinine. Signs are microalbuminuria. National Guidelines: microalbuminuria annual tests, glycemic control, regular bp check, treatment of hypertension with meds, weight loss and sodium restriction, increased risk of infection and report S&S infection symptoms to health care provider. Pt with progressive diabetic nephropathy need to explore options like dialysis and transplantation

C. Blindness and Other Visual Disordersi. Diabetes is leading cause of blindness ii. Causes: cataracts, macular degeneration and glaucoma. iii. Naional Guidelines for Diabetic Retinopathy: Report visual signs

promptly, instruct pt about relationship between hyperglycemia, hypertension and diabetic retinopathy, inform pt about importance of annual dilated exam, inform pt with isometric exercise to raise intraocular pressure (but can worse proliferative retinopathy_, inform pt about support programs and community services

D. Neuropathyi. 60-70% diabetes pt have mild/severe nervous system damage ii. Peripheral neuropathy, autonomic neuropathyiii. Autonomic neuropathy: gastroparesis, neurogenic bladder, diabetic

diarrhea, impaired CV reflex (orthostatic hypotension and tachycardia and impotence)

iv. Neurogenic bladder: frequent small voiding, incontinence leading to urinary retention

v. Cardiovascular autonomic neuropathy: resting tachycardia and orthostasis

vi. Diabetic perpheraly neuropathy- seen in legs, feet and hands vii. DPN pain first felt in the lower legs and worsens at night. Perisstent or

intermittent pain over periods of weeks or months- aching or burning. viii. Primary treatment for neuropathy is pain management

E. Vascular and Neuropathic Complications Leading to Lower Extremity Amputations

i. Low extremity amputations result from combination of pathologic events working in tandem.

ii. Testing for sensory changes in the feet of diabetic patients is done with a Semmes-Weinstein monofilament close eyes, monofilament applied to plantar surface of toes, and give a verbal cue on where it is felt. Inability means loss of protective sensation

iii. Vibratory perception threshold BPT- technique to measure sensory neuropathy. Pt indicates when he stops feeling vinbration of tuning fork. Unable to feel vibration means at risk for ulceration

iv. Conditions related to feet that are associate with higher risk for amputations: peripheral neuropathy with loss of protective sensation, altered biomechanics in presence of neuropathy, evidence of increased pressures, bony deformity, PVD, history of ulcers or amputation, severe nail pathology.

F. Charcot Deformityi. Distal symmetric polyneuropathy and peripheral autonomic neuropathy

leads to charcot deformity. ii. Autonomic neuropathy damages sympathetic nerves in small bv and

lower extremities= loss of constrictive tone, vasodilation and increased peripheral perfusion and expedited bone resorption and osteopenia

G. Gastrointestinal Disturbancesi. Gastroparesis- syndrome, impaired transit of food from stomach to

duodenum in absence of mechanical obstruction ii. Early satiety, n/v, abdonimcal discomfort iii. Fluctuations in blood glucose levels due to delayed gastric emptying or

retention of food. Hypoglycemia results from insulin peak during delayed gastric emptying. Hyperglycemia due to food absorption while insulin actions are waning

iv. Gastroparesis treatment- relies on diet and meds, nutritional support H. Diabetic Diarrhea

i. Frequent after meals and during night ii. Alternating diarrhea and constipation iii. Treatment: empirical, antdiarrheal agents

I. Oral/Dental Problems i. Receding gums, gym disease, periodontal disease, diminished saliva

production, elevated blood sugar= cavitiesii. Have good oral hygiene: brushing, flossing and rinsing

J. Complications of Pregnancyi. Elevated glucose levels in type 1 women can cause birth defects and

spontaneous abortions. ii. Chronic hyperglucemia in second and third trimester= macrosomia

(excessively large barbies)iii. Gestational diabetes- requires dietary treatment and possible insulin

therapy for hyperglycemia. Uncontrolled hyperglycemia= fetal and maternal complications. Increases risk for type 2 diabetes

K. Foot Problems i. Diabetics have high incidence of amputations of feet ii. Patient education for foot care

1. Inspection: Check feet daily 2. Daily Care: Wash feet with warm soapy water and dried

thoroughly. Soaking not advised. Lotion applied daily but not between toes

3. Footwear: Never go barefoot. Correct size. Decreased sensation in neuropathy causes unnoticed injury. Avoid garters because they restrict blood flow

4. Special care: Do NOT use OTC chemical agents to remove corns and warts. Irritation causes ulceration and sharp instruments

shouldn’t be used to self treat ingrown toenails. Notify healthcare provider if any problem arises (cut, blister, wound, infection, redness, swelling)

XIV. Health Promotion for foot problems A. ADA recommends diabetic pt receive annual thorough foot examB. Healthcare provider should assist pt in change modifiable risk factors: smoking,

home foot care, activity levels and glycemic control. C. Do not walk without shoes, walk with ill-fitting shoes, decrease attention to daily

inspection and cutting toenails if vision is too poor. D. Activities= jogging on concrete sidewalks are contraindicated E. Poor glycemic control= pour wound healing and infection

XV. Nursing ManagementA. Outpatient Management of Diabetes

i. Nurse’s role: assess insulin regimens, medication, nutrition, physical activity, adherence to guidelines and changes in health status

ii. Pt needs to have testing of A1c 2-4 times per year, ongoing MNT therapy evaluation, annual eye exam, foot exam 1-2 times per year by health care provider and daily by pt, annual nephropathy screening, regular blood pressure assessment, annual lipid profile and serum creatinine and influenza and pneumococcal immunixations. Diagnose pt needs and develop plan that includes education or referral. Ex. Nurse educates about insulin injection but refers pt for MNT. Nurse implements plan, evaluates effectiveness and modifies

B. Inpatient Nursing Management of Diabetes i. Ongoing attention to subjective and objective changes in diabetes

status (type 1 and type 2) regardless of their admitting diagnosis. ii. Nurse assesses improvement or deterioration of blood glucose iii. Nurse needs to be aware of discharge needs

XVI. Collaborative Management i. Mutlidisciplinary approach: monitor blood glucose levels, make changes

to medications and nutrition therapies and assess response to those changes

ii. Interdisciplinary team must communicate opening iii. Interdisciplinary team: Nurse, dietitian, physical therapist, health care

workerB. Health Promotion, Diabetes Education and Cultural Implications

i. Educate the patient for diabetes self-management 1. Pathophysiology of diabetes and treatments 2. Nutritional management and physical activity into lifestyle3. Use diabetes medications safely 4. Monitor blood glucose and interpret to make self-management

decisions5. Prevent, detect and treat acute/chronic complications6. Develop personal strategies to address psychosocial issues and

concerns to promote health and behavior changes ii. Culture and religious background influences values, beliefs, behaviors,

attitudes, self care habits and relationships with healthcare providersiii. Cultural Considerations: Related to Diet for Patients with Diabetes p

14571. African Americans, Asian Americans, Hispanics

XVII. Gerontological Considerations

i. Manage hyperglycemia, hypoglycemia and risk factors. Hypoglycemia, hypotension and drug interactions due to polypharmacy are of great concern.

ii. Special Considerations1. Comes from poor socioeconomic situation2. Experience greater social isolation and loneliness3. Higher frequency of depressive illness or cognitive impairment4. Nursing home 5. Relies on caregivers6. Polypharmacy7. Frail and limited life expectancy8. Comorbidities that limit ability to self medicate and recognize/ deal

with hypoglycemia 9. Factors addressed: nutrition, diet management, exercise,

medication and testing, functional impairment, cognitive impairment, emotional distress and education

B. Nutrition and Diet Managementi. Older adults are undernourished. ii. Modify diet: change nutritent composition or density, food consistency

or using supplements iii. Environmental factors need to be changed like where food is prepared,

eaten, willingness to prepare food to comply with dietary restrictions C. Exercise

i. Reduces cardiac risk and improves insulin sensitivity, improves body composition and arthritic pain, reduces falls and depression, increases strength and balance, enhances life quality and improves survival

D. Medications and Testingi. Pt and caregiver must know medication dose, route and side effects. ii. Assess physical ability to administer an insulin syringe iii. Goal is to maintain targeted glycemic control iv. Oral or multiple oral medications v. HgA1c lab testing or home monitoring

E. Functional Impairmenti. Affects ability to care for self and manage diabetes ii. Participation in activities should be encouraged and pt should be

referred to an appropriate rehab program F. Cognitive Impairment

i. In older pt with type 2 ii. Have difficulty performing self management and following complicated

treatment regimensiii. When there is nonadherance with therapy, frequent episodes of

hypoglycemia and less glycemic control= assess cognitive fxn G. Emotional Distress (Depression)

i. Associated with poor glycemic control and accelerated rates of coronary heart disease

ii. Early identification and treatment may help achieve better glycemic control

H. Educationi. Explain disease process and treatment plan, meds (type, route,

administration and seide effects), importance of physical activity and

exercise, changes in mood and behavior and knowledge of potential complications and actions to be taken

1. Determine glycemic control and evaluate conformity 2. Prevent hypoglycemia, which may lead to impaired cognition and

function3. Provide individualized counseling regarding lifestyle modification,

including med nutrition evaluation tailored to meet medical, lifestyle and personal factors

XVIII. ResearchA. Transplantation of cells responsible for insulin production and using stem cells to

regenerate pt ability to produce insulin