Nursing Management Diabetes Mellitus

Covenant School of Nursing N201 Fall, 2009 Gloria Rodriguez, MSN.RN,CDE

Objectives
By the end of this lecture students should be able to:
Differentiate between type 1 and type 2 diabetes mellitus Identify the diagnostic and clinical significance of blood glucose test results Describe the major complications of DM Differentiate between DKA and HHNS

Diabetes Mellitus
A chronic

multi-system disease related to abnormal insulin production or impaired insulin utilization.

Risk Factors
Family Hx. Of diabetes Obesity esp. abdominal and viseral adiposity. BMI> 27% Race/Ethnicity GDM or babies > 9 lbs.
Mother is more at risk of developing DM if she has big babies

HTN > 140/90 mm Hg Triglycerides > 200mg/dL Prev. impaired glucose tolerance

Causes
Genetics Autoimmune Viral Environmental

Metabolic Processes
Three Metabolic processes are important in ensuring a supply of glucose for body fuel.
1) Glycolysis-the process through which glucose is broken down into water and carbon dioxide with the release of energy

Metabolic Processes
2) Glycogenolysis- the breakdown of stored glycogen ( from the liver or skeletal muscles). This action is controlled by 2 hormones:
epinephrine-breaks down glycogen in the muscle glucagon-breaks down glycogen in the liver. Glucose from here can be directly released into the blood stream and used by the nervous system

Metabolic Processes
3) Gluconeogenesis-building of glucose from new sources.
Hormones that stimulate gluconeogensis Glucagon Glucocorticoid hormones Thyroid hormones

Process usually occurs in the liver

Normal Insulin Metabolism

Counterregulatory hormones. They work to oppose the effects of insulin. These hormones work to increase blood glucose levels by stimulating glucose production and output by the liver and decreasing the movt of glucose into the cells.
Glucagons Epinephrine Growth hormone Cortisol

Hormonal Control of Metabolism

Insulin A hormone secreted by the beta cells in the islet of Langerhans, Normally released in small increments when food is ingested. Controls blood glucose levels by regulating glucose production and storage Insulin is regulated by serum glucose levels. Consists of 2 polypeptide chains The amt of insulin a person is secreting can be tested by checking the levels of C peptide Rise in plasma insulin after a meal stimulates storage of glucose as glycogen in the liver and muscle. It also inhibits gluconeogenisis and enhances fat deposition (enhances fat to be placed/stored in the adipose tissue) in the adipose tissue and increase protein synthesis The fall in insulin levels during the night when youre not eating facilitates the release of the stored glucose from the liver, protein from the muscles and fat, and thats how it kind of compensates for your hypoglycemia

Insulin
Insulin and glucagon are hormones secreted by islet cells within the pancreas Insulin is normally secreted by the beta cells (a type of islet cells) of the pancreas Stimulus for insulin is high blood glucose levels

Hormonal Control of Metabolism

Amylin
2nd beta cell hormone Effects of Amylin
Amylin and insulin together suppress the secretion of glucagon by the liver Amylin slows the transfer of nutrients to the intestine

Continued.
Glucagon
Produced in the alpha cells of the islets of Langerhans in the pancreas Transported via the portal vein to the liver
Glucagon acts in opposition to insulin Stimulates the break-down of glycogen and fats to glucose and promotes gluconeogensis from fats and proteins

Continued.
Catecholamines
Epinephrine and norepinephrine
Help maintain glucose levels during stressful situations by
1. inhibiting insulin release and decreasing movement of glucose into cells 2. promoting glycogenolysis by converting muscle and liver glycogen to glucose 3 Increasing lipid activity, conserving energy. Causes mobilization of fatty acids and conserves glucose. The conservation of blood glucose mediated by these actions is important in the homostatic effect which occurs with hypoglycemia to increase the blood glucose levels

Continued.
Somatostatin
Produced in the pancreas by the delta cells in the islets of Langerhans
Somatostatin inhibits the secretion of insulin, glucagon and growth hormone.

Diabetes Classifications
Type 1 Type 2
Decreased sensitivity to insulin and impaired beta cell functioning which results in decreased insulin production

Gestational diabetes mellitus Pre-diabetes Secondary

Type 1 Diabetes Mellitus

Formerly Known as insulin-dependent Destruction of their pancreatic cells, genetic, immunologic, and possibly environment Persons do not inherit Type 1 itself but rather have a genetic predisposition

DCCT Study
Diabetes Control and Complications Trial (DCCT) conducted in 1993 Results showed that you can prevent the complications of diabetes.
Retinopathy Nephropathy Neuropathy Maintaining blood glucose as close to normal as possible prevents or slows the progression of long-term diabetic complications

Type 2 Diabetes Mellitus

Most Prevalent Two main problems
Insulin resistance Impaired insulin secretion Inappropriate glucose production by liver Alteration in the production of hormones and cytokines by adipose tissue.

Gestational Diabetes
Higher risk of C-section Perinatal death Neonatal complications Risk of developing type 2 DM in 5 to 10 years is increased.

Gestational Diabetes
Any degree of glucose intolerance that causes during pregnancy. Hyperglycemia develops during pregnancy- secretion of placental hormones (which causes insulin resistance)

Gestational Diabetes
High risk women should be screened at 24-28 weeks of gestation Need oral glucose tolerance test or glucose challenge A 2 hr. fasting level after 100ml glucose load of 155 would indicate GDM

Secondary Diabetes
Causes
Damage/injury/interference or destruction of pancreas Conditions
Cushing's Hyperthyroidism Recurrent pancreatitis Use of parenteral nutrition

Secondary Diabetes
Medications
Corticosteroids Thiazides Dilantin Atypical antipsychotics
Resolves when treatment of underlying condition is treated

Clinical Manifestations of Type 1 DM

Frequent urination Increase in thirst Weight loss Increase hunger Weakness

Clinical Manifestation of Type 2 Diabetes

Type 2 Non-specific Gradual Onset Include classic signs of Type 1
Most common signs of Type 2 Fatigue Recurrent infections Recurrent vaginal yeast infections Prolonged wound healing Visual changes- Blurred vision

Diagnostic Studies
Three Methods
Fasting plasma glucose level-> 126 mg-dl- no caloric intake for 8hr Random or casual plasma glucose > 200mg/dl plus S/S Two-hour OGTT level- > 200mg/dl using a 75g glucose load

Assessment
History Signs related to Dx. Of DM hyperglycemia hypoglycemia Monitor frequency, timing, severity and resolution BS monitoring Status of symptoms Adherence to Tx. Regimen Lifestyle. culture, psychosocial and economic factors Effects of complications

Assessment
Physical Exam

B/P sitting and lying-(orthostatic chg.) BMI Dilated eye exam Foot exam Skin exam Neuro. exam Oral exam

Continued
Labs
Hgb A1C
A long-term measure of glucose control that is a result of glucose attaching to hemoglobin for the life of the rbc (120 days).

Fasting lipid profile Microalbuminuria Serum Creatine UA EKG Referrals-Opthal., Podiatry, Dietician

Goal
Be an active participant To experience few or no episodes of acute hyper/hypoglycemia emergencies Maintain BS levels as close to normal Prevent, minimize or delay complications Adjust lifestyle to decrease stress

Diabetes Prevention Program

Obesity # 1 predictor of type 2 DM DPP showed a modest wt. loss of 5-10% of body wt. with regular exercise-30 min 5X/wk Dropped the risk of developing type 2 DM up to 58%

Type 2 Diabetes Mellitus

Metabolic Syndrome is increased with Type 2 DM
Characterized by:
Insulin resistance Elevated insulin levels High triglycerides Decreased HDL levels Increased LDL levels HTN

Type 2 Diabetes Mellitus

Metabolic Syndrome
Risk Factors Central obesity Sedentary lifestyle Westernization Certain ethnic groups

Five Components of Diabetes Management

Nutritional management Exercise Monitoring Pharmacologic management Education

Educators
Certified Diabetes Educators-CDE Staff Nurses
RN or LVN

Types of Insulin
Only human insulin is used Insulin's differ in onset, peak, and duration Matched to clients activity

Rapid-Acting Insulin
Humalog or Novolog (LISPRO) (Aspart) (Glulisine) Onset 10 30 min. Peak 1-2 hours. Effects last 2 hrs 6 hrs Used to
Rapidly reduce glucose level Treat postprandial hyperglycemia Prevent nocturnal hypoglycemia Usually one shot a day before each meal for a total of 3 shots a day

Short-Acting Insulin
Humilin R, Novolin R, ReliOn R Onset 30 min. 1 hr, Peak 2 4 hr Effects last 4 6 hrs Administer 20-30 mins. before eating If mixing with NPH Regular is always drawn up first.

Intermediate Acting Insulin

NPH, Novolin N, Humulin N, ReliOn N Cloudy Onset 2 4 hrs, Peak 4 14 hrs Effects last 16 24 hrs 30 mins before meal

Long-Acting Insulin
Glargine (Lantus) clear
Onset 1-2 hours Duration 12 - 24 hours No peak Cannot mix with other insulins Cannot Prefill Normally given once a day

Detemir (levemir) clear

(onset 3-4, peaks in 3-9, duration is 6-23 hours)

Both are for basil gylcemic control, doesnt control post prandial levels (levels after you eat)

Storing Insulin
Insulin can be stored at room temp. for 30 days In the refrigerator until expiration date Pre-filled pens 30 days in refrigerator Pre-filled pens with insulin mixture are usually good for 30 days

Dos and Donts of Insulin

Keep spare insulin Inspect for flocculation (frosted whitish coating) before use Avoid extreme temperatures , do not freeze Keep out of direct sunlight or in a hot car

Selecting Sites
Recommendations
Do not use same site more than once in 2-3 weeks Do not inject insulin to limb which will be used to exercise. Use same anatomic area at the same time of day

Selecting Sites
Abdomen- more stable and radid absorption Arms- posterior surface Thighs anterior surface Hips

Insulin Syringes
Syringes selected should match insulin concentration 3 types of syringes available
1 ml-holds 100 units 0.5ml-holds 50u 0.3 ml-holds 30u

Complications of insulin Therapy

Local allergic reaction( itching, erythema, and burning around inject. Site Systemic allergic reactions (urticaria and antiphylactic shock) Insulin lipodystrophy( atrophy of tissue)

Complications of Insulin Therapy

Dawn Phenomenon-hyperglycemia that is present when awakening from release of counterregulatory hormones in the predawn hours. More severe when growth hormone is peaking (Adolescence and young adulthood) Treatment- adjustment in timing of insulin or an increase in insulin

Complications of Insulin Therapy

Somogyi effect
Rebound effect overdose of insulin produces hypoglycemia During the hours of sleep Counterreglatory hormones released , stimulate lipolysis, gluocneogensis, and glycogenolysis and in turn produce rebound hyperglycemia and ketosis.

Major Classes of Medications

Thiazolidnedones & Biguanides Drugs that sensitize the body to insulin and/or hepatic glucose production Sulfonylures & Meglitnides
Drugs that stimulate the pancreas to make more insulin

Major Classes of Medications

Alpha-glucosidase Inhibitors
Drugs that slow the absorption of starches Incretin Mimetic Stimulate release of insulin, decrease glucagon secretion, increase satiey and decrease gastric emptying Amylin Analog Decrease gastric emptying , decrease glucagon secretion, decrease endogenous glucose output from liver, increase satiey

Incretin Mimetic
Byetta Exenatide
Synthetic peptide stimulates release of insulin from pancreatic B cells. Suppression of glucagon, decrease glucose from liver Slowing of gastric emptying Not indicated with insulin use Administer SubQ

Nutrition
Nutrition meal planning and weight control are the foundation of diabetes selfmanagement Need to control total caloric intake to attain or maintain a reasonable body weight and have good glycemic control

Nutrition Management Goals

Near normal blood glucose Meet energy needs Achieve lipid profile and B/P levels to reduce cardiovascular risks Improve health thru healthily food choices and exercise Cultural preferences of each individual

Nutrition Management
Weight loss is the key to treatment BMI of 25 29 is considered overweight BMI 30 is considered obese Obesity is associated with increased resistance to insulin http://www.nhlbi.nih.gov/guidelines/ obesity/bmi_tbl.htm for a BMI table

Meal Planning
Meal plans needs to be adjusted to patients ethnic background and culture. If patient is on insulin, timing and meal content can be adjusted if a person is exercising. Advances of insulin allows for more flexibility.

Meal Planning
Review patients diet history. Identify patients eating habits and lifestyle. Assess need for weight loss, weight gain, or weight maintenance.

Dietary Needs
For most diabetics a healthy diet consists of
50% to 60% of calories from carbohydrates 10-20% of calories from protein 20-30% or less of calories from fat

Carbohydrates
Recommended 50% to 60% of calories from carbohydrates Carbohydrates consist of sugars and starches Carb. counting is a useful tool for blood glucose management Low Carb. Diets are not recommended for persons with DM

Fats
Recommended fat content <20-30% of total calories Saturated fats limited to 10% total calories Limit total dietary cholesterol to <300mg per day May help reduce cholesterol levels

Proteins
Less than 10% of total energy consumed. Moderate to high protein not recommended- Too much saturated fat and unnecessary stress on kidney to excrete excess nitrogen

Fiber
Helps lower total cholesterol and lowdensity lipoprotein cholesterol in the blood Soluble and Insoluble Addition/increase of fiber in the meal plan should be gradual

Alcohol
High in calories No nutritive value Promotes triglycerdemia Promotes hypoglycemia Weight gain

Considerations
Decrease caloric intake by 500-1000 calories if client needs to lose 1-2 per week. Self-prescribed diets not good due to hormonal changes that can occur from fasting. Include increased synthesis and release of glucagons and stimulate liver glucogenalysis and could increase BS

Different Meal Plans

Carbohydrate Counting Exchange List Food Pyramid Guide Glycemic Index Portion Control Plate Method

Sweeteners
Nutritive
Contain calories Fructose (fruit sugar) Sorbitol and Xylitol

Non-nutritive
Few or no calories NutraSweet (aspartame)-4 cal. Per packet
Splenda (sucralose)

Benefits of Exercise
Lowers blood glucose
Decrease Cardiovascular risk factors. Psychological well being.

Improvement in insulin secretions.

Exercise

Lowers blood glucose

Increases uptake of glucose by body muscles Improving insulin usage Improves circulation and muscle tone

Benefits of Exercise
Lowers blood glucose Decreases cardiovascular risk factors
Improved functioning of the cardiovascular system. Improved strength and physical activity capacity Reduced risk factors of coronary artery disease

Exercise
Resistance strength training increases lean muscle mass thereby increasing resting metabolic rate. Also helps to decrease weight, decrease stress, and maintains well being.

Exercise and Cardiovascular Diseases

Alters blood lipid levels
Increases levels of high density lipo-protein (HDL) Decreases total cholesterol and triglyceride levels Important to patients with diabetes with an increase risk of cardiovascular disease.

Precautions with Exercise

Blood glucose levels > 250 mg/dl and ketones urine should not exercise until urine test negative for ketones and blood glucose levels are near to normal ( ADA, 2004).

Precautions
Exercising increases blood glucose
Exercising increases the secretion of glucagon, growth hormone and catecholamines Liver releases more glucose resulting in an increase in blood glucose level.

Type 1 and Exercise

Do not have same effect as Type 2 Hypoglycemia can occur many hours after exercise. (Up to 48 hours) due to depletion of glycogen stores is a contributing factor of hypoglycemia Food amount required varies from person to person.

Exercise and Insulin

The physiologic decrease in circulating insulin that normally occurs cannot occur in persons being treated with insulin. Need to monitor BS before, during and after exercise to determine alterations in food or insulin Food amount varies from person to person.

Carbohydrate Replacement During Exercise

Intensity Duration in Minutes CHO Replacement Frequency

Mild to Moderate

< 30

May Not Need

Moderate

30-60

15gm

Every hour

High

60+

30 to 50gm

Every hour

Type 1 and Exercise

If you are participating in long periods of exercise
Check blood sugar before, during and after exercise period and snack on carbohydrate snacks as needed to maintain blood glucose level.

Type 2 and Exercise

Obese people with Type 2
Exercise and dietary management improves glucose metabolism and enhances loss of body fat Improves insulin sensitivity and may decrease the need for insulin or oral agents.

Recommendations
Exercise at the same time each day. Exercise the same amount of time each day. If patient has diabetic complications, alter the exercise type and amount as necessary. Increased B/P assoc. with exercise may aggravate diabetic retinopathy

Recommendations
Start slow and gradually increase exercise Always discuss with physician before starting any exercise program for a medical evaluation with appropriate diagnostic studies before beginning.

Precautions with Exercise

Blood glucose levels > 250 mg/dl and ketones urine should not exercise until urine test negative for ketones and blood glucose levels are near to normal ( ADA, 2004).

Precautions
Exercising increases blood glucose
Exercising increases the secretion of glucagon, growth hormone and catecholamines Liver releases more glucose resulting in an increase in blood glucose level.

Monitoring
Blood glucose monitoring is a cornerstone in diabetes management. Self-monitoring of blood glucose (SMBG) is recommended by the ADA. Many types of glucometers-Pick the one that best suits the patient. Consider ease of use, skill level,cost of strips, visual numbers etc.

Monitoring
Potential hazards of SMBG- patients may report erroneous blood glucose values as a result of using incorrect technique.
Improper application of blood Improper meter cleaning Damage to reagent strips Coding of meter

Candidates for SMBG

Uncontrolled diabetes A tendency for hypoglycemia Hypoglycemia unawareness Patients on insulin During illness

Monitoring
According to the ADA patients on insulin should test at least four times a day, usually before meals and at bedtime. Persons not receiving insulin and on orals should test two-three times a day, including a 2hpp Important to keep a logbook and take to all doctors appointments. Persons will tend not to monitor if not taught how to use results.

Continuous Glucose Monitoring

Available Senor attached to an infusion set inserted subcutaneously in the abdomen and connected to a device worn on a belt. Worn for 72 hours and downloaded for review. Glucowatch- worn on wrist

Glycated Hemoglobin
Referred to as HgbA1c or A1C Reflects average blood glucose levels over a period of approximately 2 to 3 months, (ADA, 2004)

Acute Complications
Hypoglycemia-Abnormally low blood glucose level (<70mg/dL) Causes
Too much insulin or oral hypoglycemic agents Too little food or excessive exercise Delayed or skipped meals

Hypoglycemia
Two categories
Adrenergic
Mild hypoglycemia- sympathetic nervous system is stimulated- surge of epinephrine and norepinephrine S/S- sweating, tremor, tachycardia, palpitations, nervousness, and hunger.

Hypoglycemia
Central nervous symptoms Moderate hypoglycemia- deprives the brain cells of needed fuel for functioning S/S- inability to concentrate, headache, lightheadness, confusion, memory lapse, numbness of the lips and tongue, slurred speech, impaired coordination, emotional changes, irrational or combative behavior, double vision and drowsiness

Management/Teaching
Treat hypoglycemia using Rule of 15 Teaching Component
Teach patients to carry some form of simple sugar with them at all times. Avoid over treating hypoglycemia Consistent pattern of eating and administering of insulin.

Hypoglycemia
Emergency Measures
For patients who are unconscious or cannot swallow.
Glucagon 1mg injection can be given SubQ

Hypoglycemia Unawareness
No warning signs and symptoms of hypoglycemia Increase risk of dangerously low BS Related to autonomic neuropathy

Diabetic Ketoacidosis (DKA)

DKA caused by an absence or markedly inadequate amounts of insulin. Caused by disorders in the metabolism of fats, CHO, and proteins.

Ketoacidosis
Signs and Symptoms
Nausea and vomiting Rapid breathing Extreme tiredness and drowsiness Weakness

DKA
Three main clinical features:
Hyperglycemia Dehydration and electrolyte loss Acidosis, Brunner & Suddath.
Insulin defeiency leads to breakdown of fat ( lipolysis) into free fatty acids and glycerol. Free fatty acids are converted into ketone bodies by the liver.

DKA
Three main causes of DKA
Decreased or missed dose of insulin Illness or infection Undiagnosed or untreated diabetes Treatment
IV fluid and electrolyte replacement

DKA Treatment
Correct fluid and electrolytes Correct acidosis Provide adequate insulin Establish cause of DKA Can be mild to severe

DKA
Signs and Symptoms
Due to Na and K+ loss in urine clients experience
Muscle weakness Extreme fatigue Malaise Cardiac arrhythmias can lead to cardiac arrest Acidosis-fruity breath, tachycardia and hypotension

Monitoring and Managing Potential Complications

Fluid Overload- Administering fluids rapidly to treat DKA or HHNS Hypokalemia-due to treatment of DKA-loss of potassium Cerebral Edema-cause unknown, may be by rapid correction of hyperglycemia- resulting in fluid shift

Hyperglycemia Hyperosmolar Nonketotic Syndrome (HHNS)

Serious condition Blood glucose 800-1000 mg/dl Ketosis usually minimal or absent Defect is usually lack of effective insulin (insulin resistance) Presistent hyperglycemia causes osmotic diuresis which results in losses of water and electrolytes. To maintain osmotic equilibrium, water shifts from the intracellular fluid space to the extracellular fluid space. With glycosurea and dehydration, hypernatremia and increased osmolarity occurs. Usually occurs in older adults

Causes of HHNS
Acute illness Medications that exacerbate hyperglycemia Dialysis treatment

HHNS
Hypotension Profound dehydration Tachycardia Variable neurological signs Morality rate- 10% to 40% Treatment-fluid replacement and correct electrolytes

Comparison of DKA and HHNS

While can occur in both, usually occurs in Type 1 Precipitated by:
omission of insulin, physiologic stress (infection, surgery, etc.)

DKA

While can occur in both, usually occurs in Type 2 (esp. elderly) Precipitated by:
Physiologic stress (infection, surgery, etc.)

HHNS

Onset
Rapid (<24 hours)

Onset
Slower (over several days)

Blood Glucose Levels

Usually >250

Blood Glucose Levels

Usually > 600

Arterial pH levels
< 7.3

Arterial pH levels
Normal

Serum and urine ketones

Present

Serum and urine ketones

Absent

Serum Osmolality
300-350

Serum Osmolality
>350

BUN and Creatinine levels

Elevated

BUN and Creatinine levels

Elevated

Mortality Rate
< 5%

Mortality Rate
10-40%

Macrovascular Complications
Diseases of large and medium-size vessels Atherosclerosis- From altered lipid metabolism Cerebral Vascular Peripheral Vascular Disease Adults with DM 2-4 times increased risk of hear and cerebral vascular

Microvascular Diseases
Microvascular diseases are unique to diabetes Capillary basement membrane thickening
The basement membrane surrounds the endothelial cells of the capillary. Researchers believe that increased blood glucose levels react thru a series of biochemical responses to thicken the basement membrane to several times its normal thickness

2 areas affected
Retina kidneys

Diabetic Retinopathy
Results from chronic hyperglycemia Most common cause of new cases of blindness in persons ages 20-74 Non-proliferative-most common form Proliferative- most severe form

Retinopathy
Non-Proliferative- Partial occlusion of small blood vessels in the retina-develop microanueryms. Vision can be affected if Macula is involved. Proliferative-Retinal capillaries become occluded, hemorrhage. If blood vessels pull retina can cause a tear or partial or complete detachment of retina.

Legal Blindness
A visual acuity that is <20/200 in the better eye with corrective lenses and or a visual acuity field of < 20 degrees.

Nursing Management
Prevention is key If vision loss occurs, nursing education must address the patients adjustment to vision impairment

Medical Management
Control of blood glucose
Tight control of blood glucose reduced risk of developing retinopathy by 76% compared to that of conventional therapy

Control of hypertension Cessation of smoking

Nephropathy
Microvascular complication Damage to small blood vessels that supply glomeruli of the kidney Leading cause of end-stage renal disease
About 50% of all new ESRD cases a year are diabetics

Risk factors
HTN Genetic predisposition
Native Americans, Hispanics, and African Americans with Type 2 DM are at greater risk of developing ESRD than Whites

Smoking Chronic hyperglycemia Studies DCCT and UKPDS showed significant reduction when near-normal blood glucose control was achieved and maintained

Treatment
Aggressive B/P management with Ace inhibitor Yearly screening for microalbuminuria in the urine

Treatment of Diabetic Nephropathy

Hypertension Control - Goal: lower blood pressure to <120/80 mmHg
Antihypertensive agents
Angiotensin-converting enzyme (ACE) inhibitors
captopril, enalapril, lisinopril, benazepril, fosinopril, ramipril, quinapril, perindopril, trandolapril, moexipril

Angiotensin receptor blocker (ARB) therapy

candesartan cilexetil, irbesartan, losartan potassium, telmisartan, valsartan, esprosartan

Beta-blockers

Treatment of Diabetic Nephropathy (cont.)

Glycemic Control
Pre-prandial plasma glucose 90-130 mg/dl A1C <7.0% Peak postprandial plasma glucose <180 mg/dl Self-monitoring of blood glucose (SMBG) Medical Nutrition Therapy

Restrict dietary protein to RDA of 0.8 g/kg body weight per day

Treatment of End-Stage Renal Disease (ESRD)

There are three primary treatment options for individuals who experience ESRD:
1. Hemodialysis 2. Peritoneal Dialysis 3. Kidney Transplantation

Diabetic Neuropathy
About 60-70% of people with diabetes have mild to severe forms of nervous system damage, including:
Impaired sensation or pain in the feet or hands Slowed digestion of food in the stomach Carpal tunnel syndrome Other nerve problems

More than 60% of nontraumatic lower-limb amputations in the United States occur among people with diabetes.

Risk Factors
Glucose control Duration of diabetes Damage to blood vessels Mechanical injury to nerves Autoimmune factors Genetic susceptibility Lifestyle factors
Smoking Diet

Pathogenesis of Diabetic Neuropathy

Metabolic factors
High blood glucose Advanced glycation end products Abnormal blood fat levels

Ischemia Nerve fiber repair mechanisms

Autonomic neuropathy
Affects the autonomic nerves controlling internal organs
Peripheral Genitourinary Gastrointestinal Cardiovascular

Is classified as clinical or sub-clinical based on the presence or absence of symptoms

Continued.
Hypoglycemic unawareness Sudomotor neuropathy- absence of sweating of the extremities with a compensatory increase in upper body sweating. Sexual Dysfunction

Essentials of Foot Care

Examination
Annually for all patients Patients with neuropathy - visual inspection of feet at every visit with a health care professional

Advise patients to:

Use lotion to prevent dryness and cracking File calluses with a pumice stone Cut toenails weekly or as needed Always wear socks and well-fitting shoes Notify their health care provider immediately if any foot problems occur

Foot Care
Complications of DM contribute to an increased risk of foot infections. A foot infection is a preventable infection. Foot care measures should be practiced on a daily basis. Foot care tips-chart pg. 1287

Complications
Diabetic foot ulcers
Begins with soft tissue injury of foot. Formation of fissure between toes or in area of dry skin. Formation of callus. Ingrown toenails Cracks in skin Venous insufficiency is a contributing cause of foot ulcers

Type of Injuries
Chemical Traumatic Thermal

Foot Infections
Signs and Symptoms
Drainage Swelling Redness (cellulites of leg) Gangrene
Usually first signs of foot problem

Treatment of Foot Ulcers

Bed rest Antibiotics Debridement Good control of blood glucose (usually increases with infection).

Treatment of Foot Ulcers

If patient has PVD, ulcers may not heal due to the decreased ability of oxygen, nutrients, and antibiotics to reach the injured tissue. Amputation may be necessary to prevent spread of infection

Other Complications
Skin- Acanthosis nigricans- dark , coarse, thicken skin on the neck. Diabetic dermatopathy-red-brown flattopped papules Granuloma annulare- type 1- autoimmunepartial rings of papules, often in dorsal surface of hands and feet

Infections
More susceptible to infections Defect in the mobilization of inflammatory cells and an impairment of phagocytosis. Recurrent yeast infections Treatment must be prompt and aggressive.

Special Issues
Patient undergoing surgery
During stress such as surgery, blood glucose levels rise as a result of an increase level of stress hormones. If hyperglycemia is not controlled- osmotic diuresis may lead to excessive loss of fluids and electrolytes. Hypoglycemia- withhold SQ insulin morning of surgery

Hospitalization
Factors affecting hyperglycemia
Changes in treatment regimen Medications (eg. Glucocorticoids IV Dextrose Overly vigorous treatment of hypoglycemia.

Special Issues
Patient undergoing surgery
During stress such as surgery, blood glucose levels rise as a result of an increase level of stress hormones. If hyperglycemia is not controlled- osmotic diuresis may lead to excessive loss of fluids and electrolytes. Hypoglycemia- withhold SQ insulin morning of surgery

Hospitalization
Factors affecting hyperglycemia
Changes in treatment regimen Medications (eg. Glucocorticoids IV Dextrose Overly vigorous treatment of hypoglycemia.

Continued
Factors affecting hypoglycemia
Overuse of sliding scale Lack of dosage changes when dietary intake is changed. Overly vigorous treatment of hyperglycemia Delayed meal after lispro or aspart insulin
The chart she wants us to look at shows a stick with a wire on the end of it (a mono-filiament) being poked at 5 pressure points on the bottom of the foot (big toe, 4th toe, and 3 spots along the ball of the foot). You poke them to see if they can feel it. This is what you do when assessing the sensory threshold in pts with DM. They can also do it themselves

Alterations in Meal Plan

If client is NPO- insulin dose may need to be changed for type 2 Type 1 may need to administer insulin Frequent blood glucose monitoring. Clear liquids need to be caloric Tube feeding-important to administer insulin at regular intervals.

Promoting Self-Care
Address any underlying factors affecting diabetes control. Simplify the treatment regimen Adjust regimen to meet patients request. Provide positive reinforcement and encouragement.

Education
Flexibility is important. Teach what client wants to learn not what you think they need to learn!! The major goal of education is an educated client. Do not try to teach everything in one session.

Nursing Diagnoses
Deficient knowledge r/t diabetes self care skills/information. Potential self care deficit r/t physical impairments or social factors. Anxiety r/t loss of control, fear of inability to manage diabetes, misinformation r/t diabetes, fear of diabetes complications. Risk for infection r/t potential sensory loss in feet.

Nursing Diagnoses
Imbalanced Nutrition Related to increase in stress hormones Risk for impaired skin integrity related to immobility and lack of sensation.

Goals
Improved nutritional status Maintenance of skin integrity Ability to perform basic diabetes selfmanagement. Prevent short and long term diabetes complications