interventions for clients with diabetes mellitus 2009
TRANSCRIPT
Interventions for Clients with Diabetes Mellitus
20092009
DEFINITION
• Group of disorders• Glucose intolerance common thread
GOAL FOR NURSE
• Have patient control blood glucose levels• Prevent acute and long term complications• Develop self care habits (priority)
NORMAL ANATOMY/PHYSIOLOGY
• SOURCES OF GLUCOSE:1. From food2. From liver3. From pancreas
WHEN A MEAL IS EATEN
• Insulin secretion increases• Glucose is moved from the blood into muscle,
liver, and fat cells
INSULIN
• Hormone• Produced by pancreas• Controls level of glucose in blood• Secreted by beta cells in islets of Langerhans
in pancreas
EFFECT OF INSULIN AFTER IT IS MOVED
• Glucose is used for energy• Stimulates storage of glucose in the liver and
muscle in the form of glycogen• Promotes storage of dietary fat in adipose
tissue• Speeds up the transport of amino acids
coming from dietary protein into cells
DURING FASTING PERIODS
• Continuous release of small amount of insulin• Glucagon secreted from alpha cells of islets of
Langerhans• The liver produces glucose through
breakdown of glycogen (glycogenolysis)• After 8-12 hours the liver forms glucose from
the breakdown of noncarbohydrate substances eg: amino acids (gluconeogenesis)
STATISTICS
• About 17 million people• Cultural prevalence: Hispanics, *African
Americans, Native Americans• Costs: As of 2002 $132 billion annually for
diabetic related costs• Prevalent in elderly
CLASSIFICATION
• Type I: Characterized by destruction of pancreatic cells (beta cells die); no production of insulin
• Type II: Insulin resistance/impaired insulin secretion
• Gestational: (GDM) increased blood glucose during pregnancy
Types of Diabetes
• Other types include:– Genetic defect of beta cell or insulin action– Disease of exocrine pancreas– Drug or chemical induced (glucocorticoids, thyroid
hormone, beta-adrenergic agonists, thiazides, dilantin, etc
– Infections– Others
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TYPE 1 AND TYPE 2 DIABETESFeatures Type 1 Type 2
Former name Juvenile onsetInsulin dependent diabetes mellitus(IDDM)
Maturity onsetNon-insulin dependent diabetes mellitus (NIDDM)
Age at onset Any age, usually under 30 yr
Starts in 40’s, Peaks in 50’s; may occur earlier, increase in childhood/adolescence due to obesity
Inheritance Recessive Dominant
Nutritional status Usually nonobese 60-80% obese
Insulin All dependent on insulin Required 20-30%
Sulfonylurea therapy None Effective
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Features Type 1 Type 2
Prevalence Same for women and men
Symptoms thirst, wgt loss, None or thirst, fatigue, visual blurring, vascular or neural complications,Usually no ketoacidosis
Onset Abrupt Gradual
Medical nutrition therapy Mandatory mandatory
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Absence of Insulin
• Hyperglycemia• Polyuria• Polydipsia• Polyphagia• Hemoconcentration, hypervolemia,
hyperviscosity, hypoperfusion, and hypoxia• Acidosis, Kussmaul respiration• Hypokalemia, hyperkalemia, or normal
serum potassium levels
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Acute Complications of Diabetes
• Diabetic ketoacidosis • Hyperglycemic-hyperosmolar-nonketotic
syndrome• Hypoglycemia from too much insulin or too
little glucose
• ALL THREE PROBLEMS REQUIRE EMERGENCY TREATMENT AND BE FATAL IF NOT CORRECTED
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Chronic Complications of Diabetes
• MACROVASCULAR: large vessels– Coronary heart disease, cerebrovascular disease,
PVD, MI
• MICROVASCULAR: small vessels– Retinopathy (vision) problems– Diabetic neuropathy– Diabetic nephropathy– Male erectile dysfunction
CAUSE OF VASCULAR COMPLICATIONS
• Chronic hyperglycemia• Glucose toxicity• Chronic ischemia
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Risk for Injury Related to Hyperglycemia FIRST GENERATION SULFONYLUREA
AGENTS:• Used for clients with some pancreatic beta-
cell function, stimulate insulin secretion• Acetohexamide (Dymelor, Dimelor):• Chloropropamide (Diabinase, Novo-Propamide)• SIDE EFFECTS: **hypoglycemia common in
older, debilitated malnourished clients, CV, liver, kidney problem
– SEVERE REACTION WITH ALCOHOL: flushing, pulsating HA, sweating, confusion, slurred speed CAN LEAD TO DEATH
Risk for Injury Related to Hyperglycemia FIRST GENERATION SULFONYLUREA
AGENTS:• Tolazamide (Tolinase): give with meals to
avoid GI upset, do not give with alcohol• Tolbutamide( Orinase, Mobenoi): if client on a
beta blocker, hypoglycemia S&S masked, no alcohol
• A lot of drug interactions with this class of drug
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Chloropropamide (Diabinase, Novo-Propamide)
SECOND GENERATION SULFONYLUREA AGENTS
• Glipizide (Glucotrol): give 30 min before meals to improve absorption, don’t crush, or chew tablet, designed to be absorbed slowly, if eat low calorie increased hypoglycemia
• Glyburide (DiaBeta, Micronase): give with food decrease GI upset and enough calories to decrease hypoglycemia
• Glimepiride (Amaryl): give with 1st main meal, debilitated or malnourished clients have more hypoglycemia
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Meglitinide Analogs
• Actions and SE like sulfonylureas, rapid onset with limited duration
• HOW: lowers blood glucose by triggering insulin secretion via beta cells in 20 min
• SE: hypoglycemia• Repaglinide (Prandin): take 30 min before each
meal; best reduction of postmeal hyperglycemia• Nateglinide (Starlix): 30 min before meals, omit
med if meal skipped, add a dose if an extra meal eatenElsevier items and derived
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Biguanides
• Lowers glucose by decreasing liver glucose release and decreasing cellular insulin resistance. Does not stimulate insulin release
• Metformin (Glucopohage): give with food, check renal function, do not give with renal disease; Hold for 48 hrs before iodinated contrast materials used for radiographic tests
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Alpha-Glucosidase Inhibitors:
• Reduce hyperglycemia after meals by lowing intestinal digestion and absorption of CHO
• Inhibit enzymes in the intestinal tract delaying CHO digestion
• Acarbose (Precose); Miglitol (Glyset) • take at the first bite of each of the three main
meals, GI SE common, may accumulate in renal dysfunction, increases serum transaminase levels; NO HYPOGLYCEMIA unless given with sulfonylureas or insulin
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Thiazolidinediones
• Enhances insulin action promoting glucose utilization in peripheral tissues, called insulin sensitizers and inhibit gluconeogenesis. Can be used with sulfonylureas or insulin to improve blood glucose control
• Ploglitazone (Actos); Rosiglitazone (Avandia)• Rare cases liver failure, reduces effect of
contraceptives, SE: fluid retention, wgt gain, CHF• Liver function tests checkedElsevier items and derived items © 2006 by Elsevier Inc.
Fixed Combinations
• By combining drugs with different mechanisms of action may be highly effective in maintaining desired blood glucose control
• Some clients need combination of oral agents and insulin to control blood glucose levels
• Glucovance (Glyburide and metformin)• Avandamet (Rosiglitazone and metformin)• Metaglip (Glipizide and metformin)
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Drug Therapy
• Drug administration: started at lowest effective dose and increased every 1-2 wks until blood glucose levels are controlled
• Drug selection: age, cost, response(Continued)
RAPID ACTING iNSULINS
• Marked: NovoLog, Humalog, Apidra• Onset: 0.25-0.3 hr• Peak: NovoLog – 1-3 hrs; Humalog: 0.5-1.5
hrs; Apidra: 0.5-1.5 hrs• Duration: NovoLog – 3-5 hrs; Humalog: 3-4
hrs; Apidra: 5 hrs
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SHORT ACTING INSULIN
• Marked R on bottle for regular: Humulin R, Novolin R, Velosulin BR
• Onset: ½ hour• Peak: Humulin: 2-4 hrs, Novolin R: 2.5-5 hrs
Velosulin BR is 1-3 hours• Duration: Humulin: 6-8 hrs, Novolin R: 8hrs
Velosulin BR is 8 hrs• Usually given 20-30 minutes before a meal• May be given alone or with longer acting insulin
INTERMEDIATE ACTING INSULIN
• Eg: NPH, Lente• Onset NPH: 1.5 hrs; Lente: 2.5 hrs• Peak:NPH 4-12 hours; Lente: 7-15 hrs• Duration NPH: 24 hrs; Lente 22 hrs
LONG ACTING INSULINS
• Peakless insulin• Tends to have a long slow sustained action
rather than sharp, definite peaks, used to control fasting glucose levels
• Ultralente, lantus• Onset Ultralente 4-6 hrs: Lantus: 2-4 hrs• Peak: Ultralente: 8-20 hrs; Lantus: none• Duration : Ultralente: 24 hrs; Lantus: 24 hrs
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Insulin Regimens
• Single daily injection protocol• Two-dose protocol• Three-dose protocol• Four-dose protocol• Combination therapy
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Pharmacokinetics of Insulin
• Injection site• Absorption rate• Injection depth• Time of injection• Mixing insulins
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Complications of Insulin Therapy
• Hypoglycemia• Lipoatrophy• Dawn phenomenon• Somagyi's phenomenon
SOMOGYII PHENOMENON
• Hypoglycemia at night with hyperglycemia in morning
• Cause: too much insulin, or increase of insulin sensitivity, check exercise programs
• Treatment: gradual lowering of insulin dose and increase in diet at time of hypoglycemia reaction
DAWN PHENOMENON
• Fasting hyperglycemia results from a nighttime release of growth hormone that causes blood glucose elevations at 5-6 AM
• Common problem• Treatment: client controlled by altering time
and dose of insulin of the evening dose of (NPH) by 1-2 units
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Alternative Methods of Insulin Administration
• Continuous subcutaneous infusion of insulin • Implanted insulin pumps• Injection devices• New technology includes:– Inhaled insulin– Transdermal patch (being tested)
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Client Education
• Storage and dose preparation• Syringes• Blood glucose monitoring
Client Education: glucose self monitoring devices
• Frequent blood glucose monitoring allows the diabetic to adjust insulin to obtain optimal blood glucose control
• Detects and prevents hypoglycemia and hyperglycemia
• Maintains normal blood glucose levels decreasing long term complications
• PROTOCOL: take blood glucose 2-4 times/day
GOALS OF DIET AND WEIGHT CONTROL
• Provide all essential food constituents• Reasonable weight• Meeting energy needs• Glucose levels as close to normal as possible
with few fluctuations• Decrease serum lipid levels
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Diet Therapy • Principles of nutrition in diabetes– Protein, fats and carbohydrates, fiber,
sweeteners, fat replacers– Alcohol– Food labeling– Exchange system, carbohydrate counting
RECOMMENDED TYPES OF FOOD
• High complex carbohydrates (absorbed more gradually); eg: cereals, grains, pasta, potatoes, legumes, vegetables, and fruits
• High soluble fiber foods (oat bran cereals, beans, peas, fruits) – help control blood glucose
• Few simple or refined sugars• Limit Fats: meat, butterfat, lard, bacon, oils
GLYCEMIC INDEX
• DEFINED: description of how much a given food raises the blood glucose level compared with an equivalent amount of glucose
GENERAL GUIDELINESRELATED TO GLYCEMIC INDEX
• Combine starch foods with protein and fat foods to slow the absorption of the starch food and lower the glycemic response
• Eat raw foods to lower the glycemic response (versus chopped, pureed or cooked foods)
• Eat whole fruit to lower the glycemic response (avoid juice); the fiber slows the absorption of the food
GENERAL GUIDELINES R/T GLYCEMIC INDEX CONTINUED
• If eating simple sugar foods, eat them with food that is more slowly absorbed to lower the glycemic response to the simple sugar food
SWEETNERS
• NUTRITIVE: contain calories eg: sorbitol, xylitol
• NON NUTRITIVE: have minimal to no calories. Eg: asparatame, saccharin, acesulfame K, sucralose
• NON NUTRITIVE: approved for diabetics
MEALS
• Distribute food evenly throughout the day in 3-4 meals with snacks between meals and at bedtime
EXERCISE
• VERY IMPORTANT COMPONENT• Walking is best form• WHAT DOES IT DO? Beneficial effect on CHO
metabolism and insulin sensitivityLowers the blood glucose and reduces cardiovascular risk
• HOW? By increasing the uptake of glucose by body muscles and by improving insulin utilization
OTHER BENEFITS OF EXERCISE
• Improves circulation and muscle tone• Alters blood lipids
PROBLEMS WITH EXERCISE
• HYPOGLYCEMIA after exercise1. Eating snack after exercise and at bedtime2. Exercise at same time of day preferably
when blood glucose levels are at their peak
WHAT TO DO BEFORE EXERCISING
1. Check blood glucose levels before exercise; if exceed 250 test urine for ketones. Absence of ketones indicates enough insulin available for glucose transport
2. If ketones present client should not exercise; means current insulin levels are not adequate
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Assessment • History & Blood tests– Fasting blood glucose test: two tests > 126 mg/dL
says the client has diabetes• ADA says premeal glucose should be 80-120 mg/dL• ADA says bedtime glucose should be 100-140 mg/dl
– Oral glucose tolerance test: blood glucose > 200 mg/dL at 120 minutes ( most sensitive test for dx diabetes)
Assessment continued
Glycosylated hemoglobin assays: – nl 4-6%;– ADA says keep it at 7%– 8%or more indicate poor diabetic controlGlucosylated serum proteins and albumin (GSP &
GSA)
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Urine Tests
• Urine testing for ketones• Urine testing for renal function• Urine testing for glucose
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Whole-Pancreas Transplantation
• Operative procedure: all or part of it, or pancreas plus kidney transplant
• Rejection management• Complications• Islet cell transplantation hindered by limited
supply of beta cells and problems caused by antirejection drugs
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Risk for Delayed Surgical Recovery
• Interventions include:– Preoperative care– Intraoperative care– Postoperative care and monitoring includes care
of:• Cardiovascular• Renal• Nutritional
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Risk for Injury Related to Sensory Alterations
• Interventions and foot care practices:– Cleanse and inspect the feet daily.– Wear properly fitting shoes.– Avoid walking barefoot.– Trim toenails properly.– Report nonhealing breaks in the skin.
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Wound Care
• Wound environment• Debridement• Elimination of pressure on infected area• Growth factors applied to wounds
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Chronic Pain
• Interventions include:– Maintenance of normal blood glucose levels– Anticonvulsants: gabapentin (Neurontin)– Antidepressants:amitriptyline hydrochloride
(Elavil, Levate), nortriptyline (Pamelor)– Capsaicin cream (Axsain, Zostrix))
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Risk for Injury Related to Disturbed Sensory Perception: Visual
• Interventions include:– Blood glucose control– Environmental management• Incandescent lamp• Coding objects• Syringes with magnifiers• Use of adaptive devices
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Ineffective Tissue Perfusion: Renal
• Interventions include:– Control of blood glucose levels– Yearly evaluation of kidney function– Control of blood pressure levels– Prompt treatment of UTIs– Avoidance of nephrotoxic drugs– Diet therapy– Fluid and electrolyte management
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Potential for Hypoglycemia• Blood glucose level < 70 mg/dL• Diet therapy: carbohydrate replacement• Drug therapy: glucagon, 50% dextrose,
diazoxide, octreotide• Prevention strategies for:– Insulin excess– Deficient food intake– Exercise– Alcohol
MILD HYPOGLYCEMIA• Blood sugar drops to less than 60 mg/dL• Sympathetic nervous system stimulate; Surge of
adrenalin• Causes sweating, tremor, tachycardia,
palpitations, nervousness, hunger, shaky, headache, fully conscious
• TREAT with 10-15 g of CHO, glucose tablets or gel, fruit juice, regular soft drink, 8 oz of skim milk, 6-10 hard candies, 4 cubes of sugar, 6 saltines, 3 graham crackers, 1 tblsp of honey or syrup
MODERATE HYPOGLYCEMIA
• Blood sugar drops: to 40 mg/dL• Deprives brain cells of fuel• Impaired function of CNS• Cold, clammy skin, pale, rapid pulse, rapid
shallow respirations, marked change in mood• Treat with 15-30 g of rapidly absorbed CHO• Take additional food such as low fat milk or
cheese after 10-15 min
SEVERE HYPOGLYCEMIA
• CNS CHANGES SO IMPAIRED NEED HELP• UNABLE TO SWALLOW, UNCONSCIOUSNESS,
CONVULSIONS• BLOOD GLUCOSE USUALLY LESS THAN 20
MG/Dl• TREATMENT: 1 MG OF GLUCAGON AS im OR
SUB q, ADMINISTER A SECOND DOSE IN 10 MINUTES IF STILL UNCONSCIOUS, GO TO ER
HYPOGLYCEMIA CONTINUED
• Late food after insulin administration• Excessive insulin dose
GUIDELINE TO PREVENT HYPOGLYCEMIA:
FEED THE PEAK
DIABETIC KETOACIDOSIS
• CAUSED by absence of insulin, illness, infection, initial S&S of undiagnosed untreated DM
• RESULTS in disorders in metabolism of CHO, protein and fat
• 3 MAIN FEATURES: dehydration, electrolyte loss, acidosis
DKA
• Not enough insulin leads to• Decreased amount of glucose entering cells• Leads to liver making lots of glucose• RESULTS: hyperglycemia• Kidneys try to help by excreting glucose, but
water and electrolytes get lost too (Na and K)
DKA CONTINUED
• Excessive urination leads to DEHYDRATION AND MARKED ELECTROLYTE LOSS
• In response to decreased insulin fats breakdown to FATTY ACIDS and GLYCEROL
• The liver converts free fatty acids into KETONE BODIES
• KETONE BODIES (are acids) accumulate and lead to METABOLIC ACIDOSIS
DKA CONTINUED
• Blood glucose could be 300 to 800 or 1000 or higher
• KETOACIDOSIS reflected in following:– Low serum bicarb (0-15)– Low pH (6.8 to 7.3)– Low PCo2 (10-30)– REFLECTS RESPIRATORY COMPENSATION FOR
METABOLIC ACIDOSES
DKA CONTINUED
• Na and K may be low, normal or high depending on the water loss
• High creatinine, high BUN, high Hgb, High Hct seen with dehydration
TREATMENT OF DKA
• DEHYDRATION: rehydrate; may need 6-10 liters of NSS, 1 liter/hour for 2-3 hours then change to ½ NS
• ELECTROLYTE LOSS: K may be low, normal or high initially, but there is a major loss of K during the dehydration; give 40 mEq KCl/hour for several hours
TREATMENT OF DKA CONTINUED
• ACIDOSIS: insulin IV at slow rate 5 units/hour• Hourly blood glucose levels
MATH OF INSULIN DRIPS
• Nurse must convert hourly rates of insulin infusion to IV gtt rates
• Eg: 100 units Regular insulin mixed in 500cc of 0.9 NS
• 1 unit of insulin = 5 cc• Order is 5 units per hour• MATH: 5 units x 5 cc = 25 cc/hour
INSULIN DRIPS
• Infuse separately to allow for frequent changes
• When mixing insulin drip, flush insulin solution through the entire IV infusion set and discard the first 50 cc fluid
• WHY: inuslin molecules adhere to glass and plastic infusion sets, thus initial fluid has a decreased concentration of insulin
INSULIN DRIPS
• Always run insulin continuously otherwise ketone bodies return
• Even if blood glucose drops or returns to normal, keep insulin going
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Potential for Hyperglycemic-Hyperosmolar Nonketotic Syndrome and Coma
• Interventions include:– Monitoring– Fluid therapy: to rehydrate the client and restore
normal blood glucose levels within 36 to 72 hr– Continuing therapy with IV regular insulin at 10
units/hr often needed to reduce blood glucose levels
SICK DAY RULES
• Call MD• Blood glucose q 4 hr• Urine for ketones when blood glucose is
greater than 240 mg/dl• Take insulin/oral antidiabetic agents• Drink 8-12 oz sugar free liquids q hour awake• Eat regular meals• Call doctor for mod/lg ketones, N/V,
uncontrolled blood glucose, high feverElsevier items and derived items © 2006 by Elsevier Inc.