diabetes. Management ppt can use for nursing

Diabetes

1. Nursing Management
Diabetes Mellitus
Covenant School of Nursing
N201 Fall, 2009
Gloria Rodriguez, MSN.RN,CDE

2. 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

3. Diabetes Mellitus
•A chronic multi-system disease
related to abnormal insulin
production or impaired insulin
utilization.

4. 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

5. Causes
•Genetics
•Autoimmune
•Viral
•Environmental

6. 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

7. 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

8. 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

9. Normal Insulin Metabolism
•Counterregulatoryhormones. 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 movtof glucose into the
cells.
–Glucagons
–Epinephrine
–Growth hormone
–Cortisol

10. 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
gluconeogenisisand 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 you’re not eating
facilitates the release of the stored glucose from the liver, protein
from the muscles and fat, and that’s how it kind of compensates
for your hypoglycemia

11. 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

12. Hormonal Control of Metabolism
•Amylin
–2
nd
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

13. 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

14. 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

15. 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.

16. 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

17. 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

18. 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”

19. 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.

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

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

23. 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

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

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

26. Clinical Manifestations of Type
1 DM
•Frequent urination
•Increase in thirst
•Weight loss
•Increase hunger
•Weakness

27. 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

28. 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

29. 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

30. Assessment
•Physical Exam
–B/P sitting and lying-(orthostatic chg.)
–BMI
–Dilated eye exam
–Foot exam
–Skin exam
–Neuro. exam
–Oral exam

31. Continued…
•Labs
–HgbA1C
•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

32. 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

33. 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%

34. 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

35. Type 2 Diabetes Mellitus
•Metabolic Syndrome
–Risk Factors
•Central obesity
•Sedentary lifestyle
•Westernization
•Certain ethnic groups

36. Five Components of Diabetes
Management
•Nutritional management
•Exercise
•Monitoring
•Pharmacologic management
•Education

37. Educators
•Certified Diabetes Educators-CDE
•Staff Nurses
–RN or LVN

39. Types of Insulin
•Only human insulin is used
•Insulin's differ in onset, peak, and duration
•Matched to client’s activity

40. 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

41. 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.

42. 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

43. 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 gylcemiccontrol, doesn’t
control post prandiallevels (levels after you
eat)

44. 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

45. Do’s and Don’ts 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

46. 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

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

48. 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

49. 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)

50. 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

51. 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.

52. 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

53. 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

54. 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

56. Nutrition
•Nutrition –meal planning and weight
control are the foundation of diabetes self-
management
•Need to control total caloric intake to attain
or maintain a reasonable body weight and
have good glycemic control

57. 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

58. 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.htmfor a BMI table

59. Meal Planning
•Meal plans needs to be adjusted to
patient’s 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.

60. Meal Planning
•Review patient’s diet history.
•Identify patient’s eating habits and
lifestyle.
•Assess need for weight loss, weight gain,
or weight maintenance.

61. 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

62. 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

63. 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

64. 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

65. Fiber
•Helps lower total cholesterol and low-
density lipoprotein cholesterol in the blood
•Soluble and Insoluble
•Addition/increase of fiber in the meal plan
should be gradual

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

67. 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

68. Different Meal Plans
•Carbohydrate Counting
•Exchange List
•Food Pyramid Guide
•Glycemic Index
•Portion Control
•Plate Method

69. Sweeteners
•Nutritive
–Contain calories
–Fructose (fruit sugar)
–Sorbitol and Xylitol
•Non-nutritive
–Few or no calories
–NutraSweet (aspartame)-4 cal. Per packet
–Splenda (sucralose)

71. Benefits of Exercise
•Lowers blood glucose
•Decrease Cardiovascular risk factors.
•Psychological well being.
•Improvement in insulin secretions.

72. Exercise
•Lowers blood glucose
–Increases uptake of glucose by body muscles
–Improving insulin usage
–Improves circulation and muscle tone

73. 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

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

75. 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.

76. 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).

77. 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.

78. 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.

79. 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.

80. 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

81. 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.

82. 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.

83. 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

84. 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.

85. 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).

86. 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.

88. 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….

89. 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

90. Candidates for SMBG
•Uncontrolled diabetes
•A tendency for hypoglycemia
•Hypoglycemia unawareness
•Patients on insulin
•During illness

91. 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 doctor’s appointments.
•Persons will tend not to monitor if not
taught how to use results.

92. 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

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

95. 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

96. 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.

97. 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

98. 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.

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

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

101. 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.

102. Ketoacidosis
•Signs and Symptoms
–Nausea and vomiting
–Rapid breathing
–Extreme tiredness and drowsiness
–Weakness

103. 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.

104. 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

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

106. 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

107. 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

108. Hyperglycemia Hyperosmolar
Nonketotic Syndrome (HHNS)
•Serious condition –Blood glucose 800-1000 mg/dl
•Ketosis usually minimal or absent
•Defect isusuallylack of effectiveinsulin (insulin
resistance)
•Presistenthyperglycemia 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 glycosureaand dehydration,
hypernatremiaand increased osmolarityoccurs.
•Usually occurs in older adults

109. Causes of HHNS
•Acute illness
•Medications that exacerbate
hyperglycemia
•Dialysis treatment

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

111. Comparison of DKA and HHNS
DKA
•While can occur in both, usually
occurs in Type 1
•Precipitated by:
–omission of insulin, physiologic
stress (infection, surgery, etc.)
•Onset
–Rapid (<24 hours)
•Blood Glucose Levels
–Usually >250
•Arterial pH levels
–< 7.3
•Serum and urine ketones
–Present
•Serum Osmolality
–300-350
•BUN and Creatininelevels
–Elevated
•Mortality Rate
–< 5%
HHNS
•While can occur in both, usually
occurs in Type 2 (esp. elderly)
•Precipitated by:
–Physiologic stress (infection, surgery,
etc.)
•Onset
–Slower (over several days)
•Blood Glucose Levels
–Usually > 600
•Arterial pH levels
–Normal
•Serum and urine ketones
–Absent
•Serum Osmolality
–>350
•BUN and Creatininelevels
–Elevated
•Mortality Rate
–10-40%

113. 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

114. Microvascular Diseases
•Microvasculardiseases 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

115. 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

116. 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.

117. 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.

118. Nursing Management
•Prevention is key
•If vision loss occurs, nursing education
must address the patient’s adjustment to
vision impairment

119. 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

120. 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
•

121. 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

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

123. 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

124. •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 Diabetic
Nephropathy (cont.)

125. 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

126. 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.

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

128. Pathogenesis of Diabetic
Neuropathy
•Metabolic factors
–High blood glucose
–Advanced glycation end products
–Abnormal blood fat levels
•Ischemia
•Nerve fiber repair mechanisms

129. 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

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

131. 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

132. 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

133. 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

135. Type of Injuries
•Chemical
•Traumatic
•Thermal

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

137. Treatment of Foot Ulcers
•Bed rest
•Antibiotics
•Debridement
•Good control of blood glucose (usually
increases with infection).

138. 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

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

140. 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.

141. 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

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

143. 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

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

145. 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 lisproor aspartinsulin
•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, 4
th
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 pt’s with DM. They
can also do it themselves

146. 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.

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

148. 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.

149. 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.

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

151. Goals
•Improved nutritional status
•Maintenance of skin integrity
•Ability to perform basic diabetes self-
management.
•Prevent short and long term diabetes
complications