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Compare the age of onset, clinical manifestations, and pathologic mechanisms of Type I diabetes.
Discuss nursing interventions for the client with hypoglycemia, hyperglycemia, DKA.
List the onset and peak times of various insulins.
Develop a teaching plan for a Type I diabetic client.
Identify, discuss, and describe the physical and emotional needs of the client who has Type I diabetes and the client's family.
Discuss the ethical challenges involved in caring for a noncompliant Type I diabetic client.
Major complications of Diabetes
Hypertension and hyperlipidemia
Two types of islet cells important to glucose control are
alpha cells, which secrete glucagon, and the beta cells, which produce insulin and amylin.
Is a "counterregulatory" hormone that has actions opposite those of insulin. It prevents hypoglycemia by triggering the releaes of glucose from cells storage sites. Insulin prevents hyperglycemia by allowing body cells to take up, use, and store carbohydrate, fat, and protein.
40 to 50 unites of insulin is secreted daily directly into liver circulation in a two-step manner. It is secreted at low levels during fasting (basal insulin secretion) and at increased levels after eating (prandial). An early burst of insulin secretion occurs within 10 minutes of eating. This is followed by an increasing release that lasts until the blood glucose level is normal.
Type 1 Diabetes
+beta-cell destruction leading to absolute insulin deficiency
Type 2 Diabetes
+Ranges from insulin resistance with relative insulin deficiency to secretory deficit with insulin resistance
Gestational Diabetes Mellitus
+Glucose intolerance with onset or first recognition during pregnancy
Main fuel for central nervous system cells. Because the brain cannot produce or store much glucose, it needs a continuous supply from circulation to prevent neuronal dysfunction and cell death.
Is the most efficient means of storing energy. Fat has 9 calories of stored energy per gram
Protein and carbohydrates
Have only 4 calories per gram
The main metabolic effects of insulin
Are to stimulate glucose uptake in skeletal muscle and heart muscle and heart muscle and to suppress liver production of glucose and very-low-density lipoprotein.
In the liver, Insulin
Promotes the production and storage of glycogen breakdown into glucose (glycogenolysis). It increases protein and lipid (fat) synthesis and inhibits ketogenesis (conversion of fats to acids) and gluconeogenesis (conversion of proteins to glucose).
Insulin in muscle
Promotes protein and glycogen synthesis.
Insulin in fat cells
It promotes triglyceride storage.
Insulin in the fasting state
(not eating for 8 hours), insulin secretion is suppressed, which leads to increased gluconeogenesis in the liver and kidneys, along with increased glucose generation by the breakdown of liver glycogen. In the fed state, insulin released from pancreatic beta cells reverses this process
When more glucose is present in liver cells than can be metabolized for energy or stored as glycogen
Insulin causes the excess glucose to be converted to free fatty acids. These FFAs are deposited as fat in fat cells.
Physiologic Response to Insufficient Insulin
+Decreased glycogenesis (conversion of glucose to glycogen)
+Increased glycogenolysis (conversion of glycogen to glucose)
+Increased gluconeogenesis (formation of gluvose from non-carbohydrate sources, such as amino acids and lactate)
+Increased lipolysis (breakdown of triglycerides to glycerol and free fatty acids)
+Increased ketogenesis (formation of ketones from free fatty acids)
+Proteolysis (breakdown of protein with amino acid release in muscle)
Lack of Insulin
Lack of insulin in the body or bad receptors, prevents some cells from using glucose for energy. The body then breaks down fat and protein in an attempt to provide energy and also increases the levels of counterregulatory hormones in an attempt to make glucose from other sources.
Classic symptoms of diabetes:
Is frequent and excessive urination and results from an osmotic diuresis caused by excess glucose in the urine. As a result of diuresis, sodium, chloride, and potassium are excreted in the urine and water loss is severe.
What plyuria causes
Dehydration results, and polydipsia (excessive thirst) occurs. Because the cells receive no glucose, cell starcation triggers polyphagia (excessive eathing.
Despite eating cast amounts of food, the preson remains in starvation until insulin is available to move glucose into the cells.
With indulin deficiency, fat break down, releasing free fatty acids. Conversion of fatty acids to ketone bodies provides a backup energy source. They have abnormal breakdown leading to metabolic acidosis.
Dehydration that occurs with diabetes leads to
+hemoconcentration (increased blood concentration)
+Hypovolemia (Decreased blood volume)
+Hyperviscosity (thick, concentrated blood)
+poor tissue perfusion
+Hypoxia (poor tissue oxygenation), especially to the brain.
Due to the increase of CO2 and H+, what do they trigger
These products trigger the respiratory centers of the brain to increase the rate and depth of respiration in an attempt to excrete more carbon dioxide and acid. Called Kussmaul repiration. Acetone is exhaled, giving the breath a "fruity-shity" odor.
Insulin lack initially causes potassium depletion. With the increased fluid loss from hyperglycemia, excessive potassium is excreted in the urine, leading to low serum potassium levels. Depending on the hydration, people with DM may have hypo-, hyper, or normal Potassium levels.
Acute complications of Diabetes
+Diabetic ketoacidosis (DKA) caused by lack of insulin and ketosis
+Hyperglycemic-hyperosmolar state (HHS) caused by insulin deficiency and profound dehydration.
Hypoglycemia from too much insulin or too little glucose
-All three problems require emergency treatment and can be fatal if treatment is delayed or incorrect.
Include coronary heart disease, cerebrovascular disease, and peripheral vascular disease, lead to increased early death.
+Microvascular complications of blood vessel structure and function lead to nephropathy, neuropathy, and retinopathy.
Chronic hyperglycemia causes
Thickining basement membranes, which causes organ damage
Glucose toxicity affects
Directly or indirectly affects functional cell integrity
Chronic ischemia in small blood vessels causes
Connective tissue hypoxia and microischemia
Additional risk factors that contribute to poor health outcomes for people with DM include
Smoking, physical inactivity, increased body weight, hypertension, and excessive blood levels of cholesterol and other fats.
DM affects the heart muscle, causing both systolic and diastolic heart failure. Left ventricular dysfunction with heart failure and fatal cardiac dysrhythmias are more common after MI in patients with DM
Cardiovascular risk factors associated with DM
Obesity, hypertension, dyslipidemia, and sedentary lifestyle.
C-Reactive protein (CRP)
Patients with DM often have higher levels of C-reactive protein, an acute-phase inflammatory marker associated with increased risk for cardiovascular problems and death.
Eye and vision complications in DM
Blindness is more common in patients with diabetes. Diabetic retinopathy is strongly related to the duration of diabetes.
-After 20 years of DM, nearly all patients with type 1 disease and most with type 2 disease have some degree of retinopathy.
Nonproliferative diabetic retinopathy
+Causes structural problems in retinal vessels, including areas of poor retinal circulation, edema, hard fatty deposits in the eye, and retinal hemorrhages.
Diabetic macular edema
is characterized by increased blood vessels permeability and deposits of hard exudates at the center of the retina. This problem is the main cause of vision loss in the person with DM.
Is a progressive deterioration of nerves that results in loss of nerve function. It is a common complication of DM and often involves all parts of the body. Damage to sensory nerve fibers result in either pain or loss of sensation. Damage to motor nerve fibers results in muscle weakness. Damage to nerve fibers in the autonomic nervous system can cause dysfunction in every part of the body.
Hyperglycemia leads to
Neuropathy thorugh blood vessels changes that cause nerve hypoxia. Both the axon and its myelin sheath are damaged reduced blood flow, resulting in blocked nerve impulse transmission.
Are the most common neuropathies in DM and involve widespread nerve function loss. They have a slow onset, affect both sides of the body, involve motor and sensory nerves, progress slowly, are permanent, and include autonomic nerve dysfunction. Late complications include foot ulcers and deformities.
Affect a single nerve or nerve group and usually are caused by an acute ischemic event or by nerve trapping. Both problems lead to nerve damage or nerve death.
Manifestations of focal neuropathies
Beging with pain on one side of the face near the affected eye. The eye muscles become paralyzed, resultig in double vision. Problem usually resolves in 2 to 3 months.
Type 1 Diabetes
Is an autoimmune disorder in which beta cells are destroyed in a genetically susceptible person. The immune system fails to recognize normal body cells as "self" and takes destructive actions againt them. Immune system cells, mediators, and antibodies attack and destroy insulin-secreting cells in the islets.
What may cause Type 1 Diabetes
Certain viral infections, such as mumps and coxsackievirus infection, appear to trigger autoimmune destruction of pancreatic beta cells.
+Low vitamin D levels
Exposure to the Epstein Barr virus, mumps virus
Timing of introducing cereal into baby's diet - best if done at 3-7 months
Type 1 diabetes (Former names)
Juvenile-onset diabetes, Ketosis-prone diabetes, Insulin-dependent diabetes mellitus
Type 1 diabetes (Age of onset)
Usually younger than 30 yr, occurs at any age
Type 1 diabetes (Symptoms)
Abrupt onset, thrist, hunger, increased urine output, weight loss
Type 1 diabetes (Etiology)
Type 1 diabetes (Pathology)
Pancreatic beta-cell destruction
Type 1 diabetes (Antigen pattners)
Type 1 diabetes (Antibodies)
ICAs present at diagnosis
Type 1 diabetes (Endogenous insulin and C-peptide)
Type 1 diabetes (Nurtritional status)
Type 1 diabetes (Insulin)
All dependent on insulin
Type 2 diabetes (former names)
Adult-onset diabetes, ketosis-resistant diabetes, non-insulin-dependent diabetes mellitus
Type 2 diabetes (Age at onset)
Peaks in 50s; may occur earlier
Type 2 diabetes (Symptoms)
Frequently none; thirst, fatigue, blurred vision, vascular or neural complications
Type 2 diabetes (pathology)
Insulin resitance, dysfunctional pancreatic beta cell
Type 2 diabetes (nutrictional status)
60 to 80 % obese
Type 2 diabetes (Insulin)
Required fo 20 to 30 %
Type 2 Diabetes
Is a progressive disorder in which the person has a combination of insulin resistance and decreased secretion of insulin by pancreatic beta cells. Insluin resistance develops from obesity and physical inactivity in a genetically susceptible person.
What is type 2 diabetes accompanies by
Other cardiovascular risk factors of hyperlipidemia, hypertension, and increased clot formation.
Heredity and type 2 dm
Plays a major role in the development of type 2 dm.
Metabolic syndrome (Syndrome X)
Is the simultaneous presence of metabolic factors known to increase risk for developing type 2 DM and cardiovascular disease.
Type I Diabetes Symptoms
CNS symptoms of diabetes (-) means more common in type 1
-Kussmaul breathing (hyper-ventilation)
-Smell of acetone
Fasting blood sugar (no diabetes, pre-diabetes, diabetes)
Under 100 (no diabetes)
126 and above (Diabetes)
Random blood sugar (no diabetes, pre-diabetes, diabetes)
Under 140 (no diabetes)
Over 200 with symptoms (Diabetes)
defined as impaired fasting glucose (IFG) or impaired glucose tolerance (IGT).
+Criteria for impaired fasting glucose (IFG) is 100-125 mg/dL
Instructions to patients going to do a fasting plasma glucose tolerance test
No food or drink 8 to 12 hours prior to test
Health Promotion and Maintenance of diabetes 1
No interventions are successful in preventing type 1 DM. Health promotion for patients with type 1 DM focuses on controlling hyperglycemia to reduce its long-term complications.
Health promotion and maintenance of Diabetes 2
Adopting a low-calorie diet that results in weight loss and increasing physical activity.
Lab Assessment of Diabetes
+Normal A1C 4-6%
+A1C of 6.5% or higher (Glycosylated hemoglobin, hemoglobin a1c, hgba1c)
+Levels >8%= poor diabetic control
+Never share glucose monitoring equipment
+Built in memories, pt keeps log
+Newest ones - minimal amount of blood
+Insurances will pay for most equipment
+Frequent calibration needed
+Observe patient's monitoring technique
+In Type I - after diagnosis, need very little insulin to control glucose. Even as insulin islet cell antibodies destroy B-cells, B-cells continue to produce insulin.
+Period may last up to a year.
+Patients may believe that they were misdiagnosed
Acute Complications of Type I
2. Hypoglycemia from
too much insulin or
too little glucose
Symptoms of DKA
N & V
Dehydration with orthostatic changes
Kussmaul breathing with fruity breath
Testing for DKA, Test for ketones if:
+Blood sugar is higher than 240 mg/dl on a glucose meter
+Sick with the flu or food poisoning and vomiting, Test for ketones every four to six hours, since ketoacidosis is more likely to develop
+Do not exercise if ketones present
to prevent DKA
+May substitute CHO liquids jello, pop
+Continue with insulin. Extra insulin may be necessary
+BS at least every 4 hours
+Check for ketonuria if BG > 240 mg/dL
+Increase fluids - 8 to 12 oz /hr for adults
+Continue to eat meals if able
+If surgery, insulin drip and IV fluids
for DKA,Call MD if:
+Blood glucose > 240
+Moderate or large ketones
+BG elevation after 2 doses of insulin
+Fever over 101.5 or fever longer than 24 hrs
+Ketonuria lasting more than 24 hours
+Client cannot take food or liquids
+Illness lasts more than 1 to 2 days
+Persistent nausea and vomiting
(symptoms) Potential for Hypoglycemia
Blood glucose level <70 mg/dL
Blood Sugar Mnemonics:
Shaky, sweaty - take sugar
Hot & Dry = Sugar High
Cold and Clammy = Need some
Causes of Hypoglycemia
+Takes too much insulin (or an oral diabetes medication that causes your body to secrete insulin)
+Does not eat enough food
+Exercises vigorously without eating a snack or decreasing the dose of insulin beforehand
+Waits too long between meals
+Drinks excessive alcohol, although even moderate alcohol use can increase the risk of hypoglycemia in people with type 1 diabetes
Early (Mild) signs of hypoglycemia
Late (Moderate to severe) signs of hypoglycemia
Treatment of hypoglycemia (Mild-early symptoms)
+Patient will be able to self-treat
Treatment of hypoglycemia (Moderate-late symptoms)
+Patient may need assistance to treat
+Oral glucose if able to cooperate and swallow
+Glucagon by injection if unresponsive or unable to cooperate
Treatment of hypoglycemia (Late symptoms)
+Patient will need assistance to treat
+Glucagon by injection if no intravenous access
+Intravenous glucose if preferred
Foods Containing 15 Grams of Carbohydrates (Mild hypoglycemia)
+ 3-4 glucose tablets
+ 1 tube prepackaged glucose gel
+1/2 cup fruit juice
+1 cup reduced fat milk
+ 1 cup regular (not diet) soda
+ 2 tablespoons of raisins
+ 1 tablespoon syrup
+ 10 rolled hard candy such as Lifesavers
Treating severe hypoglycemia
Rapid acting insulin
+Insulin aspart (Novolog) Onset- 5-15 minutes
+Insulin glulisine (Apidra) Onset-
+Human lispro injection (Humalog) Onset-
Complications of Insulin Therapy: Lipoatrophy, Lipohypertrophy
Lipohypertrophy: Repeated needle injections into the same site can create hardened tissue or fatty deposits called lipohypertrophy (see above).
Lipoatrophy: a breakdown of subcutaneous fat at the site of an insulin injection. It usually occurs after several injections at the same site.
Complications of Insulin Therapy: Dawn Phenomenon
+Abnormal early-morning increase in blood sugar usually between 5 a.m. and 6 a.m.
+Caused by overnight release of hormones that increase insulin resistance.
+Manage by increasing overnight insulin targeted at early morning hours
+Check 2 am glucose
Complications of Insulin Therapy: Somogyi Phenomenon
Is morning hyperglycemia from the counterregulatory response to night time hypoglycemia. It is managed by ensuring adequate dietary intake at bedtime and evaluating the insulin dose and exercise programs to prevent conditions that lead to hypoglycemia.
followed by hyperglycemia
May experience HA
Manage by preventing nocturnal hypoglycemia
Check 2 am blood glucose
Glycosylated hemoglobin (HBA1C) test
Test that measures how much glucose permently attaches to a specific area of the hemoglobin molecule. Levels greater than 6.5% is the diagnostic for DM.
Detect for ketone bodeis. Urine testing for ketones should be performed during acute illness or stress, when blood glucose levels consistently exceed 300 mg/dL, during pregnancy, or when any symptoms of ketoacidosis are present.
Tests for kidney function
Urine albumin excretion rates of 20 to 200 g/min indicate microalbuminuria.. In patients with nephropathy, a rise in serum creatinine level is related to both poor blood glucose control and hypertension.
Drug therapy for Type 1 and 2
Type 1 is only insulin.
Type 2 is insulin and oral anti diabetic drugs. These drugs are not a substitute for dietary modification and exercise. Teach the patient about the need for continuing dietary restrictions and regular exercise while taking antidiabetic drugs.
Increase insulin secretion
Side effects -
Reduce hepatic production and tissue sensitivity
Side effects -
GI side effects (diarrhea, N &V, abdominal pain)
Use caution with renal, liver or cardiac disease
NURSING SAFETY PRIORITY: Metformin
Can cause lactic acidosis in patients with renal insufficiency and should not be used by anyone with kidney disease.
Insulin lispro, insulin aspart, and insulin glulisine
Have rapid onsets of time when blood glucose is in the target range. If hyperglycemia or hypoglycmia is not present, these insulins can be given at any time from 10 minutes before mealtime to just before eating or even immediately after eating.
Should be given at least 20 to 30 minutes before eating when glucose levels are within the target range. When blood glucose levels are above the target range, the lag time should be increased to permit insulin to begin to have an effect sooner.
Can be given 15 minutes before and regular insulin 30 to 60 minutes before eating a meal. WHen blood glucose levels are below the target range, injection of regular insulin should be delayed until immediately before eating and injection of rapid-acting insulin should be delayed until sometime after eating the meal.
When rapid-acting (Humalog or NovoLog) or short (regular) insulin is mixed with a longer-acting insulin
Draw the shorter-acting dose into the syringe first.
Should not be mixed with any other forms of insulin because of the low pH of its diluent
When rapid-acting insulin is mixed with either an intermediate-acting or a long-acting insulin,
The mixture should be injected within 15 minutes before a meal
NURSING SAFETY PRIORITY-mixing
Do not mix any other insulin type with insulin glargine, insulin detemir, or with any of the premixed insulin formulations, such as humalog mix
Problems with insulin pump (CSII)
Skin infections if needle not changed every 2 to 3 days. When the patient is receiving rapid-acting insulin and has normal blood glucose levels, stopping the infusion quickly results in hyperglycemia.
Storing insulin in refrigerator
Insulin should not be allowed to freeze. Insulin glargine (Lantus) should be stored in a refrigerator even when in use.
Accuracy of the blood glucose monitor
Is ensured when the manufacturers directions are followed. The most sifnificant soure of error in blood glucose measurement is related to the skill of the user and not to errors of the intrument.
Continuous glucose monitoring
Is meant to supplement, not replace, finger stick tests. Insulin should be given only after confirming the results of any of the contnuous glucose monitoring systems.
Carbohydrate recommendation for the patient with diabetes
Is a diet containing 45% to 65% of calories from carbohydrate, with a minimum intake of 130 g carbohydrate/day. The diet should include carbohydrate from fruit, vegetables, whole grains, legumes, and low-fat milk. Diets restricting total carbohydrate to less than 130 g/day are not recommended in the management of diabetes.
Intake of 15% to 20% of total daily calories is appropriate for patients with diabetes and normal kidney function. In patients with microalbuminuria, reducing protein intake to 10% of calories may slow more than.08 g/kg body weight in later stages of chronic kidney disease may improve function.
Improves carbohydrate metabolism and lowers cholesterol levels. The American Heart Association recommends a fiber intake of 25 g each day.
Adding high-fiber foods to the diet gradually can reduce abdominal cramping, loose stools, and flatulence. The nurse and the patient should pay careful attention to blood glucose levels because hypoglycemia can result when dietary fiber intake increases significantly.
Include sucrose and a variety of nonnutritive substances. Dietary sucrose does not increase blood glucose more than equal amounts of other starches. Intake of sucrose and sucrose-containing foods by patients with diabetes does not need to be restricted out of a concern for causing hyperglycemia.
Levels are not affected by moderate use of alcohol when diabetes is well controlled. Two OH beverages for men and one for women with meal plan. Alcohol raises plasma triglycerides. Thus reducing or abstaining from alcohol is important for patients with hyperlipidemia.
NURSING SAFETY PRIORITY-alcohol
Because of the potential for alcohol-induced hypoglycemia, instruct the patient with diabetes to ingest alcohol only with or shortly after meals.
Physical exercise and hypoglycemia
Physical exercise can cause hypoglycemia if insulin is not decreased before activity. For planned exercise, reduction in insulin dosage is the preferred method for hypoglycemia prevention. For unplanned exercise, intake of additional CHO is usually needed.
Type 1 diabetes and weight, Hyperinsulinemia
It is important for patients with type 1 diabetes to avoid gaining weight.
Can occur with intensive treatment schedules and may result in weight gain. These patients may need to manage hyperglycemia by restricting calories rather than increasing insulin.
Exercise therapy for type 2 and type 1
Regular exercise is an essential part of diabetic management. Exercise does not result in hyperglycemia or hypoglycemia.
Type 1 DM cannot make the hormonal changes needed to maintain stable blood glucose levels during exercise. Without an adequate insulin supply, cells cannot use glucose. Low insulin levels trigger release of glucagon and epinephrine to increase liver glucose production, further rasing blood glucose levels. Exercise in the patient with uncontrolled diabetes results in further hyperglycemia and the formation of ketone bodies. He/she may have prolonged elevated blood glucose levels after vigorous exercise.
Exercise and hypoglycemia
Exercise in the person with diabetes can cause hypoglycemia because of increased muscle glucose uptake and inhibited glucose release form the liver.
Benefits of exercise for type 1
Appropriate exercise results in better regulation of blood glucose levels and lowering of insulin requirements. Exercise also increases insulin sensitivity, which enhances cell uptake of glucose and promotes weight loss.
Exercise adjustments for complications of diabetes
Vigorous aerobic or resistance exercise may be contraindicated in the presence of proliferative diabetic retinopathy or severe nonproliferative diabetic retinopathy. Teach the patient with retinopathy to avoid the valsalva maneuver (breath holding while bearing down) and activites that increase blood pressure.
Recommendations of exercise
The positive benefits of exercise are short term. Advise people with DM to perform at least 150 min/week of moderate intensive aerobic physical activity, or 75 min/week of vigorous aerobic physical activity or both.
Recommendations of exercise to type 2 diabetes
Patients with type 2 DM are urged to perform resistance exercise 3 times a week, targeting all major muscle groups.
When urine ketones are present (for exercise)
When urine ketones are present, the patient should NOT exercise. Ketones indicate that current insulin levels are not adequate and that exercise would elevate blood glucose levels. CHO foods should be injested to raise blood glucose levels above 100 before engagin in exercise.
NURSING SAFETY PRIRITY-Exercise
Teach patietns with type 1 diabetes to perform vigorous exercise only when blood glucose levels are 100 to 250 mg/dL and no ketones are present in the urine.
Teaching patient about exercise
Teach patients not to exercise within 1 hour of insulin injection or at the peak time of insulin action. Exercise can increase absorption of insulin from the injection site, increaseing blood insulin levels. The risk for hypoglycemia increases when insulin is injected into an area that is exercised.
Teach patient to have a candy bar or some sort of sugar before, and with him just in case of hypoglycemia.
Most effective method for achieving glycemic targets in the intensive care setting.
Continuous IV insulin solutions.
Most effective method for non-critically ill patients
Scheduled subcutaneous injection with basal, meal, and correction elements.
When a patient is NPO
Administration of rapid-acting or short-acting insulin, as well as amylin and incretin mimetics, will cause hypoglycemia if a patient is not eating.
Basal insulin should be administered when the patient is NPO because it treates baseline glucose levels. Insulin mistures are not administered because they contain some short-acting or rapid-acting insulin and will cause hypoglycemia.
Is the most common complication of diabetes leading to hospitalization.
The major causes of diabetic foot ulcers
Are peripheral neuropathy and ischemia from peripheral vascular disease.
Autonomic neuropathy causes
Loss of normal sweating and skin temperature regulation, resulting in dry, thinning skin. Skin cracks and fissures increase the risk for infection. Sensory neurpathy may cause tinglin or burning, but more often it produces numbness and reduced sensation. Without sensation, the patietn does not notice injuries to the foot and dose not treat them.
How can foot injuries occur
Walking barefoot, wearing ill-fitting shoes, sustaining thermal injuries from heat (hot water...) Because the blood supply to the diabetic foot is poor, these injuries can lead to amputation.
Prevetio of high-risk conditions
Neuropathy of the feet and legs can be delayed by keeping blood glucose levels as near normal as possible. Poor blood glucose control increases the risk for neuropathy and amputation. Intensive therapy reduces the risk for peripheral sensory neuropathy by 60%. Urge smoking cessation to reduce the risk for vascular complications.
Risk factors for ulcers or amputation
+Increase duration of diabetes.
+poor glucose control
+cardiovascular, retinal, or kidney complications.
Proper Foot Care
Clean feet with mild soap
Trim nails straight across
Use moisturizing lotion
Examine feet daily. Use mirror to look at sole of each foot
See provider as soon as lesion is detected
Invest in well fitting shoes -wear socks
Foot care - see podiatrist
Wound Care; Wound environment
Wound environment-Is influenced by the dressing. Antiseptics such as providone iodine, hydrogen peroxide, and chlorhexidine interfere with wound healing. Dressings that keep the wound moist are essential.
Wound Care; Debridement
Removes dead tissues that support bacterial growth. Mechanical debridement, although helpful, can delay healing by removing newly formed tissue.
Wound Care; Eliminating pressure
On an infected area is essential to wound healing. Teach patients with foot ulcers to not wear a shoe on the affected foot while the ulcer is healing. Teach patient that foot ulcers will recur unless weight is permanently redistributed.
Wound care; Growth factors
Applied to wounds increase healing by stimulating new tissue and enhancing cell growth.
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