Chapter 41

Diabetes Mellitus
Diabetes Mellitus - a group of diseases that are characterized by hyperglycemia due to:
Defects in - Insulin secretion, insulin action, or both.
Patho:

Glucose = energy.
Absorption of ingested food in the GI tract converted by the liver = glucose
Insulin is secreted by the Beta cells in the Pancreas - required for glucose metabolism.
A person eats = > insulin secretion = glucose moves from blood and into muscle, liver and fat cells.
o > insulin secretion especially with carbohydrates
o Glycogen glucose

Function of insulin:
o Transport and metabolize glucose for energy
o Stimulate storage of glucose in the liver and muscle as glycogen
o Signals liver to stop release of glucose.
o Enhances storage of dietary fats in adipose tissue
o Inhibits the breakdown of stored glucose, protein and fat.

< BS = glucagon released from alpha cells (pancreas) = breakdown of glycogen (liver) = glucose released.
Glucagon activates gluconeogenesis where non carb substrates like amino acids are converted to
glucose from the liver= another source of glucose,
o After 8-12 hours without food
o Glucagon is inhibited with high BS levels.
Diabetes interferes with insulin, leading to increased levels of glucose(hyperglycemia)
So
o >BS (from eating) =beta cells release insulin (alpha cells quiet)
o < BS = <insulin secretion = alpha cells active = glucagon released into blood.
o Beta cells active hyperglycemia
o Alpha cells active - hypoglycemia

S/S

DM is characterized by the 3 Ps:

o Polydipsia (increased thirst)
o Polyuria (increased urine output)
Due to excess loss of fluid associated with osmotic diuresis.
o Polyphagia (increased appetite)
Due to catabolic state induced by insulin deficiency and breakdown of proteins and fats.
Tingling or numbness in hands or feet
Fatigue, weakness, vision changes (blurred vision)
Slow healing skin lesions/wounds, dry skin
Recurrent infections

Risk factors for DM (generally type 2)

Familial History
HTN > 140/90
Obesity (20% over desired body weight or BMI > 27.)
Low HDL < 35 mg/dl
Race (AA and Hispanics are highest at risk)
Triglycerides >250
Hx of gestational diabetes
Age > 45yrs
o With elderly, > BS appears in the 5th decade of life and > withFasting
age. glucose problems

Classifications of DM

Type 1 Diabetes (Autoimmune) non insulin producing

o Destruction of the pancreatic beta cells = < insulin production, unchecked glucose production by
liver, and hyperglycemia.
o Upon diagnosis
Patient usually thin or have recent/sudden weight loss.
Onset acute and usually before 30yrs.
o Patient needs lifelong insulin !!
o Risk Factor
Genetic Predisposition, immunologic and possibly environmental (viral) factors.
o Type 1 diabetes will never move to another category of DM.
o Without Insulin production:
Glucose from food isnt stored by the liver and is unable to enter cells for metabolism = it
stays in blood stream after eating = hyperglycemia.
No inhibition of glycogenolysis (so more glucose is made) = further hyperglycemia
If BS exceeds the renal threshold for glucose (180 mg/dl-200 mg/dl), kidneys may not
reabsorb all the filtered glucose and it appears in the urine as Glycosuria.
o Glycosuria = fluids and electrolytes will follow = Osmotic Diuresis.
Fat breakdown occurs = > Ketone bodies (byproduct of fat breakdown).
This can result in a life threatening complication - Diabetic Ketoacidosis
o DKA
Absence of insulin
Body continues to breakdown stored glucose & produce new glucose from amino acids.
= further hyperglycemia eeek!!
Resulting fat break down = ketone bodies release (= acids disturbs acid base balance)
S/S
FRUITY BREATH
Abdominal pain, N, V, hyperventilation, change in LOC to coma.
Treatment
Fluid and electrolytes and INSULIN!

Type 2 Diabetes (most common kind)

o Most common in:
> 30yrs and obese (risk factors stated above)
o Slow, progressive glucose intolerance, may go undetected for years, leading to increased long
term complications such as eye disease, peripheral neuropathies, and PVD.
o Main problems with type 2 are insulin resistance and impaired insulin secretion.
Due to Beta cells working overtime = increased amounts of insulin in order to maintain
glucose level at normal or slightly elevated.
This is known as Metabolic Syndrome
HTN, hypercholesterolemia, and trunkal obesity.
If beta cells cannot keep up with demand, glucose levels rise and Type 2 develops.
o Mild S/S
Fatigue, irritability, N/T in hands and feet
Poorly healing skin, dry skin
Vaginal infections
Polyuria, polydipsia, and blurred vision (if glucose is very high).
o Treatment:
Initially with diet and exercise, then possibly oral hypoglycemic and insulin.
o May move to another category of DM. HHNS linked with Type 2 diabetes

Gestational Diabetes(Usually develops in 2-3rd trimester)

o Any degree of glucose intolerance with the onset during pregnancy.
o Secretion of placental hormones = insulin resistance = hyperglycemia.
o The development of GD increases risk for hypotensive disorders.
o High Risk pts
Marked obesity, previous GD, glycosuria, or strong familial history
Should be blood screen at first prenatal visit.
If not done initially, then test at 24-48 weeks gestation.
o All women should be tested at 24-28 weeks gestation.
o Post birth, GD will go away but woman will be at > risk to develop type 2 DM later in life.
Pt should be counseled to maintain ideal body weight and exercise regularly to < risk.
o Diagnosis
Oral glucose tolerance test ot glucose challenge test
o BS:
< 105 pre prandial
< 130 post prandial at least 2 hours post meal
o Treatment:
Diet, BS monitoring, insulin during pregnancy.

Pre-Diabetes
o Condition which BS falls between normal and those considered dx for DM.
o Previous history of hyperglycemia
o Impaired Glucose intolerance
BS = 140 199 = pre diabetic with oral glucose tolerance test.
o Impaired fasting > 40 yrs with family hx or S/S.
BS = 110 125 = pre diabetic with fasting test
o Treatment weight control 1st then diet and exercise.
Weight loss of 10-15lbs can delay onset and improve glycemic control.

Diagnostic
Abnormally high BS = basic criteria for dx of Diabetes.
o Symptoms of Diabetes (polyuria, polydipsia, polyphagia)
PLUS Casual plasma glucose concentration (Random BS) > 200 mg/dl
OR
o Fasting plasma glucose > 126 mg/dl - (NPO 8 hrs)
OR
o Oral glucose tolerance test - 2 hour post eating glucose > 200 mg/dl
This one is generally used in gestational diabetes
Hemoglobin A1C
o Blood test that is reported as a % - used to screen and dx DM.
Diabetics aim < 7%.
Normal people= 4-6%
o Monitors the control of glucose/diabetes over 3 month period
o If diagnosed for DM- recommended to have twice a year
Medical Management
Main goal:
o Normalize insulin activity and blood glucose levels (BGL) to reduce the development of vascular
and neuropathic complications.
Retinopathy, nephropathy, neuropathy.
Intensive treatment

Dramatically < vascular and neuropathic complications

Includes 3 or 4 insulin injections per day or continuous SubQ insulin infusion pump
Frequent BGM
Weekly contracts with diabetic educators.
Therapeutic goal is to achieve euglycemia (normal BGL) without hypoglycemia while maintaining high
quality of life.
o Normal blood glucose level = 70-100
5 management components are: nutrition, exercise, BG monitoring, medications and education.
1. Nutrition:
Nutrition, meal planning and weight control are the foundation of DM management.
o Control of total caloric intake for good body weight
o Control BGL and normalize lipids and BP to prevent heart disease.
o By controlling this you can reverse hyperglycemia in type 2 DM.
o Registered Dietician to design and teach this to Pt.
For obese pts, especially type 2, weight loss is key to treatment. If this pt requires insulin
or oral meds to control BGL, weight loss may reduce or eliminate need for meds.
DO NOT skip meals = increased demand on pancreas.
Consistent meal content or timing is recommended.
Measure serving sizes
Snacking may help prevent hypoglycemic reactions and maintain overall BG.
Higher intake of carbs rather than fat or proteins
Grains = 6 -11 servings
Carbs have the greatest effect on BG.
Veg = 5 - 6
Daily
Carbs = 50-60 %, emphasizing whole grains. Fruit = 2 - 4
Milk & dairy = 2 - 3
Servings
Fat = 20-30%
Meat
=
4oz
From
Protein = 10-20%
Fats
=
1
serving
ADA
25 grams of fiber should be ingested daily.

Soluble fiber (legumes, oats and some fruits) lowers BG and Lipid levels more than
insoluble.
Insoluble Fiber(whole grain breads, some cereals and veggies) keeps you fuller
longer(helps with weight loss).
Fiber <LDL and total chol and improve BS so you dont get spikes.

Exchange list: 6 main ones

List of foods for meal planning.
Each contains equal numbers of calories and are equal in g of protein, fat, carbs.
6 Main ones: Bread/starch, Vegetable, Milk, Meat, Fruit, and Fat
Glycemic Index
Describes how much food > BS
Combine starchy food with protein and fat containing food to slow absorption
and lower glycemic response.
Raw and whole foods results in lower glycemic response
o Rather than cooked, chopped or pureed
Whole fruit rather than drinking juice (it has fiber = slower absorption)
Eat foods that contain sugar with foods that are more slowly absorbed.
ETOH recommended at
Women = 1 alcoholic beverage/day
Men = 2 alcoholic beverages/day
Drinking ETOH on an empty stomach = hypoglycemia so drink with food!!!
Nutritive sweeteners such as fructose, sorbitol and xylitol cause < elevation than sucrose.

 Nonnutritive sweeteners such as saccharin, aspartame, Sunnette and Splenda.

2. Exercise
< BS level by putting glucose back into cells (less in bloodstream)
Aids in weight loss, lowers cardiovascular risk.
Weight lifting can increase lean muscle mass and increase metabolic rate
> HDL
< Cholesterol and triglycerides in blood
Slow, gradual increase in exercise period is encouraged. Walking is great!
Weight loss of 10-15lbs is a huge help
Exercise same time daily, preferably when BGL are at peak and also regularly rather than
sporadically.
Pts who are > 30yrs and have 2 or more risk factors for heart disease need an exercise
stress test. Risk factors include: HTN, Obesity, high chol. Levels, smoking, family history, etc.
Exercise precautions:
Patients with BS > 250 mg/dl and have ketones in urine shouldnt exercise. (BS could increase)
Pts who require insulin should eat
A 15 carb snack (fruit)
A snack of complex carbs with a protein
before engaging in moderate exercise to prevent hypoglycemia.
May also need to consume snack at end of exercise (as well as bedtime) to avoid post
exercise hypoglycemia, which can occur hours later.
Use proper footwear.
Avoid exercise in extreme heat or cold
Inspect feet daily after exercising
Avoid exercise during periods of poor metabolic control

3. Blood Glucose Monitoring

Self-Monitoring Blood Glucose(SMBG)
Most methods involve obtaining a drop of blood from fingertip, applying it to a special
reagent strip and letting it stay for about 5-30 seconds. The meter will give a digital
readout of the BG value.
Plasma Glucose Values are 10-15% higher than whole blood glucose values and pts
should know which one their monitor reads.
Potential hazard of SMBGs are using incorrect technique and getting an erroneous BG
reading.
Common mistakes are improper application of blood to strip (too little),
damage to reagent strips caused by heat or humidity, outdated strip, and
improper meter cleaning and maintenance.
Important for Nurse to observe pt techniques!
Every 6-12 months pts should conduct a comparison of their meter result
with a lab measured BGL in their drs office to ensure accuracy.
Candidates for SMBG are those with unstable diabetes, tendency to develop severe
ketosis or hyperglycemia and hypoglycemia without warning symptoms.
Patient should have: good visual acuity, good cognition, and manual dexterity(fine
motor skills) to use SMBG
Type 2 diabetic, SMBG recommended during periods of
Suspected hyperglycemia (illness)
Hypoglycemia

When meds or dosage of meds are modified.

Frequency: 2-4x daily (usually before meals and at bedtime).
For pts who take insulin before each meal, testing is required at least 3x daily
before each meal to determine dose.
For those who DO NOT take insulin should test at least 2-3x per week,
including a 2 hour post prandial test.
Patient should keep a log or record in order to detect patterns.
To evaluate need for dosage adjustments: test at peak action of time of med
To evaluate basal insulin and determine bolus dose: test before meals
To determine bolus doses of regular/rapid acting insulin: test 2 hrs post meal.
Pts with type 2 DM are encouraged to test daily before and 2 hours after
largest meal of the day until stabilized. After, testing should be done
periodically before and after meals.
Pts who take insulin at bedtime or use and insulin infusion pump should also
test at 3am once a week to ensure BGL isnt decreasing overnight.
Baseline patterns should be established for 1-2 weeks.

Testing for Ketones

Urine dipstick(Ketostix or CHemstip uK)
Reagent strip turns purple if ketones are present in urine.
Should be performed whenever
o Pt with type 1 DM has glycosuria
o Persistently elevated BS > 240mg/dl for 2 testing period in a row
o Illness, Gestational Diabetes and preg with preexisting diabetes.

4. Medications

Insulin Therapy

SMBG is a cornerstone of this kind of therapy.

Insulin vary according to 3 main characteristics:
Time course of action, Species (Source), Manufacture

Rapid acting:
Rapid onset - instruct pt not to eat more than 5-15 minutes before administration.
Some pts with type 1, type 2 or gestational may also require a long acting(basal) insulin to
maintain glucose control.
Short acting aka Regular:
Only insulin approved for Iv use
Clear solution
Administered 20-30 min before a meal
Intermediate aka NPH or Lente:
May Function as Basal Insulin
But need to be split into 2 injections to achieve 24 hour coverage.
White and Cloudy
If taken alone, not crucial to be taken 30 min before a meal
Important that pts eat food around the time of onset and peak of these insulins.
Very Long lasting aka peakless - LANTUS:
FDA approved as basal insulin
Can be administered once/day and is absorbed very slowly over the course of 24 hours
Comes in a suspension with a pH of 4 and cannot be mixed with other insulins

Must be taken at the same time every day - recommended in the morning.

Time Course of Action

Time Course
Rapid Acting

Short Acting
Aka Regular

Agent
Lispro (Humalog)

Onset
10-15 min

Peak
1 hour

Duration
2-4 hours

Aspart (Novolog)

5-15 min

40-50 min

2-4 hours

Glulisine (Apidra)

5-15 min

30-60 min

2 hours

Regular
(Humalog R,

- 1 hour

2-3 hours

4-6 hours

2-4 hours

4-12 hours

16- 20
hours

Novolin R,
Iletin II Regular)
Intermediate
Acting

NPH-Nuetral
Protamine
Hagedorn

(Humalin N,
Iletin II Lentin,

Indications
Used for rapid < BS,
to treat post prandial
hyperglycemia, and/or
to prevent nocturnal
hypoglycemia
Instruct pt to eat within 5-15
minutes after injection.
Usually administered 20-30 min
before a meal; may be taken
alone or in combination with a
longer acting insulin.
Clear solution.
Usually taken after food
White and cloudy

4-12 hours
3-4 hours

16-20
hours

Iletin II NPH,
Novolin L,
Novolin N)
Very Long
Acting

Glargine(Lantus)
Detemir (Levemir)

1 hour

Continuous- 24 hours
no peak

Used for basal dose

Never mix with anything

NI: Emphasize which meals and snacks are being covered by which insulin doses
Rapid and short acting cover increase in glucose after meals(immediately after injection),
Intermediate covers subsequent meals
Long lasting provide constant level.
Insulin pumps calculate basal rate too.
Insulin Regimens
Usually 1-4 injections/day
Usually combination of short and longer acting insulin
2 General approaches:
o Conventional
1 or more injections of a mixture of short acting and intermediate acting insulins per day.
Patient should not vary meal patterns and activity level
Best for terminally ill, elderly, or those who are unable/unwilling to engage in selfmanagement activities that are part of a more complex regimen.
o Intensive
More control over glucose levels

More flexibility: allows pt to change insulin does from day to day in according to eating
and activity patterns.
Reduces risk of complications however pts on this regimen are at 3x more at risk for
severe hypoglycemia
Not recommended for pts who:
Had kidney transplant
Nervous system disorders
Recurring severe hypoglycemia
Irreversible diabetic complications such as blindness or end stage renal disease
Cerebrovascular or cardiovascular disease
Ineffective self-care skills

Complications of insulin therapy

Local Allergic Reaction
o Redness, swelling tenderness and induration or a 2-4cm wheal may appear at injection site 1-2
hours after injection
o Will disappear with continued use
o Dr may prescribe an antihistamine to be taken 1 hour before injection
Systemic Allergic reaction
o Rare but will start as a local reaction then spread to hives.
o Usually associated with generalized edema or anaphylaxis
o Treatment is desensitization-small increasing amounts of insulin
Insulin Lipodystrophy
o Localized reaction in the form of lipoatrophy (loss of subcutaneous fat) which appears as slight
dimpling or serious pitting of subq fat or lipohypertrophy (fibro fatty masses at injection site).
o Lipohypertrophy is caused by repeated use of an injection site this is why its important to rotate
sites.
Resistance to injected insulin
o Defined as daily insulin requirement of 200 units or more
o Most common cause for this is obesity
Morning Hyperglycemia
o Is caused by insufficient insulin overnight.
o This can be due to:
Dawn Phenomenon
Normal BS until 3 am then it rises (hyperglycemia)
Change time of evening injection later - from dinner to bedtime
Administer intermediate or long lasting insulin
Somogyi Effect
Nocturnal hypoglycemia followed by rebound hyperglycemia
Treated by decreasing evening dose or increasing bedtime snack
Insulin waning
Progressive increase in BS from bedtime to morning.
Treated by increasing evening dose
o Testing at bedtime, 3am and upon awakening done to provide dosing info
Methods of insulin Delivery
Insulin Pen
o Small (150-300 unit) prefilled insulin cartridge.
o Best if only need to inject 1 kind of insulin at a time or who can use the premixed insulins.
o Convenient for those with manual dexterity(fine motor) probs, visual probs, etc..
Jet injectors

o Insulin absorbed faster via this method

o May cause bruising
Insulin Pumps-uses only rapid acting insulin
o Small externally worn device (needle inserted into sub q tissue, usually abdomen)
o Delivers continuous subq infusion of insulin at a basal rate of 0.5 to 2.0 units/hour
o 3 ml syringe attached to long thin tube with a needle or Teflon catheter attached to end
o Needle or cath is changed every 3 days
o Disadvantages are :
Disruptions to insulin flow from obstruction or if needle or tubing become occluded
Potential infection.
o Most common risk is ketoacidosis, which occurs if occlusion in set or pump = hyperglycemia.
o Benefit is that it can be removed for sex and stuff..best for pts with hectic lifestyle and no risk for
DKA from disruption of flow for pts with type 2 diabetes.

Insulin Teaching to pts

Storing Insulin
o Should be refrigerated and temp extremes should be avoided.
o Do not allow to freeze
o Never keep in direct sunlight or car.
o When preparing to use, let insulin get to room temp to avoid irritation to injection site.
o If a vial of insulin will be used within 1 month, may be kept at room temp.
o Pt should always have spare vial
o Cloudy insulins should be thoroughly mixed by inverting or rolling between hands prior before
being drawn up. (clear to cloudy NPH)
o Bottles of intermediate acting insulin should be inspected for flocculation (frosted whitish coating
inside bottle).
Occurs mostly in human insulins that have been exposed to temp extremes.
Do not use if this is present!!!!!!!!!!!!
Selecting Syringes
o Syringe Sizes: 1ml holds 100 units, 0.5 ml hold 50 units, and 0.3 ml holds 30 units..
o Most syringes have a disposable 27-29 gauge needle that is approximately 0.5 inch long.
o Small insulin needle (31 gauge, 8 mm) used for children or very thin pts
Mixing Insulins
o When mixing insulins, ADA recommends regular insulin be drawn up first.
(CLEAR Regular TO CLOUDY NPH)
o Never inject cloudy insulin into clear vial = contaminates entire vial of clear and alters its action.
o Premix insulin commonly comes in ratio of 70/30 (70 NPH and 30 regular)
Combo is available as Novolin 70/30 and Humulin 70/30.
o Prefilled syringes should be kept in fridge and be stored with the needle in an upright position to
prevent clogging. Should also be thoroughly mixed prior to injection.
Withdrawing Insulin
o Inject bottle with air amounting to equivalent number of units of insulin to be withdrawn.
Injection sites
o Four main injection sites are
Abdomen, upper arms (posterior Surface), thighs(anterior surface), and hips.
o Speed of absorption is greatest in abdomen.
o Always rotate to prevent lipodystrophy
Patient should not use same site more than once in 2-3 weeks

1.
2.
3.
4.
5.

If going to exercise, pt shouldnt inject into limb that will be exercised as can cause drug to be
absorbed faster, leading to hypoglycemia!!!
o Preferable for patient to use same anatomic area at same time of day consistently as it reduces
day to day variation in blood glucose levels cause by different absorption rates.
Skin prep
o Though use of alcohol is not recommended, be sure to allow skin to completely dry if you do use
alcohol, Otherwise is may lead to irritation.
Needle injection
o For normal or overweight person, a 90 degree angel is best.
o Aspiration of needle is NOT recommended.
Injection
With one hand, stabilize skin by spreading it or pinching up a large area
Pick up syringe with other hand and hold it as you would a pencil. Insert needle straight into skin 90 deg.
To inject insulin, push plunger all the way in.
Pull needle straight out of skin and press cotton ball over injection site for a few seconds
Use disposable syringe only once and discard.

Oral Antidiabetic agents

May be effective for type 2 DM that can be treated with MNT(medical nutrition therapy) and exercise alone.

1st Generation Sulfonylureas

o Acetohexamide (Dymelor)
o Chlorpropamide(diabbinese)
o Tolazamide (Tolinase)
o Tolbutamide (orinase)
Used in type 2 to control BG.
Stimulate beta cells of pancreas to secrete insulin
S/E
o Hypoglycemia
o Mild GI
o Weight gain
o Sulfa allergy
o Skin reactions
o Interacts with warfarin, Nsaids and sulfonymides
NI
o No alcohol
o High risk for hypoglycemia
o Monitor BG and urine Ketone levels to assess effectiveness of therapy
nd
2 Generation
o Glipizide (Glucotrol)
o Glyburide (Micronaise Diabeta)
o Glimepiride (Amaryl)
Used in type 2 to control BG.
Stimulate beta cells of pancreas to secrete insulin
More potent and can be used in combo with metformin or insulin to improve glucose
control.
S/E
Same as 1st gen but NO skin allergy
NI

Same as 1st gen but if taken with beta blocker, may mask s/s of hypoglycemia

Biguanides
o Metformin (Glucophage)
Used in type 2 DM.
Inhibit production of glucose by liver
Increase body sensitivity to insulin
Decrease hepatic synthesis of cholesterols
S/E
Lactic Acidosis
Hypoglycemia if used with insulin or other antidiabetic drugs
GI disturbance
Dont give to pts with impaired renal or liver function, respiratory insufficiency,
and severe infection or alcohol abuse.
NI
Monitor renal function
Pts taking metformin are at increased risk of acute renal failure and lactic acidosis
with use of ionated contrast material for contrast study so metformin should be
stopped 48 hours prior to an 48 hours post use of contrast agent or until renal
function is evaluated and normal.

Alpha-Glucosidase Inhibitaors
o Acarbose (Precose)
Used in type 2 DM
Delays absorption of complex carbs in the intestine and slows entry of glucose into
systemic circulation
Do not increase insulin secretion
Can be used alone or combined with sulfonylureas, metformin or insulin to improve
glucose control
S/E
Hypoglycemia
GI
Drugs
NI
Must be taken with first bite of food to be effective
Monitor liver function studies every 3 months for 1 year then periodically.
Do not use in opts with GI or renal dysfunction or cirrhosis.
Hypoglycemia must be treated with glucose and NOT sucrose

Non-Sulfonylurea Insulin Secretagogues

o Repaglinide (prandin)
Used in type 2 DM.
Stimulates pancreas to secret insulin
Can be used alone or in combo with metformin or thiazolidinediones to improve glucose
control.
S/E
Hypogylcemia/ weight gain - less than with sulfonylureas
Drug interactions
NI
Has rapid action and short half life

Take before each meal - only if able to eat meal immediately

Teach pt symptoms of hypoglycemia
Thiazolidinediones aka glitazones
o Rosiglitazone (Avandia)
Sensitize body tissue to insulin; stimulate insulin receptor sites to lower blood glucose
and improve action of insulin
May be used alone or in combination with sulfonylureas, metformin or insulin.
S/E
Hypoglycemia
Anemia
Weight gain, edema
Decrease effectiveness of oral contraceptives
Possible liver dysfunctions
Hyperlipidemia
Impaired platelet function
NI
Monitor BG
Monitor Liver function tests
Arrange dietary teaching to establish weight control program

All these drugs are to be used in addition to MNT and exercise not a substitution.
May need to be halted temporarily if hypoglycemia develops that is attributed to infection, trauma or
surgery.
50 percent of all pts who start out on oral antidiabetics will eventually need insulin (secondary failure).
o Primary failure is when BG remains high 1 month after initial med use.

5. Teaching
Know S/S of hypo/hyperglycemia
Diet Log
Weight Log
Glucose Log
Inspect Feets
Stress = >glucose production

Acute Complications

1. Hypoglycemia
o
o
o

BS < 50-60 mg/dl

Often occurs before meals, especially if snacks are omitted or meals are delayed.
Causes:
Too much insulin or oral hypoglycemic agent
Too little food
Excessive physical activity
S/S
Sweating
Tremors
Due to Mild Hypoglycemia
Tachycardia
< BS stimulates SNS to release epinephrine and
Palpitations
norepinephrine resulting in these side effects
Nervousness
(adrenergic symptoms)
Hunger

Inability to concentrate
Headache
Light headedness, drowsy
Confusion and Memory lapses
Numbness of tongue and lips
Slurred speech
Double vision
Irrational or combative behavior

Disoriented behavior
Seizures
Difficulty arousing from sleep
Loss of consciousness

Due to Moderate Hypoglycemia

CNS is impaired due to inadequate BGL
in brain cells

Due to Severe Hypoglycemia

CNS function is very impaired

Treatment
15 g of a fast acting carb such as:
3 or 4 commercially prepared glucose tablets.
4-6 oz fruit juice or regaulr soda
6-10 hard candies
2-3 teaspoon sugar or honey

Retest BS in 15 min and retreat if its less than 79-75 mg/dl.

If symptoms still persist > 10-15 minutes post initial tx, tx is repeated even if BS testing isnt possible.

Once symptoms resolve, a snack containing protein and starch (milk or cheese and crackers)is
recommended unless pt plans to eat a regular meal or snack within 30-60 minutes.

In an emergency situation For adults who are unconscious and cant swallow 1. Injection of Glucagon 1mg can be given sub q or IM.
Injectable Glucagon is packaged as powder and must be mixed with a dilutant
immediately before being injected.
Pt may take 20 min to regain consciousness.

 Duration of 1mg glucagon is brief: onset 8-10 min and action lasts 12-27
minutes.
Give pt concentrated source of carb followed by a snack upon awakening to prevent
reoccurrence of hypoglycemia.
Some pt may experience nausea post injection so turn pt to side to prevent aspiration if
vomiting occurs.

2. 25-50 ml of 50% Dextrose solution IV in the event of an emergency too.

Effect seen within minutes.
Patient may complain of headache and pain at injection site.
Assure patency of IV line as hypertonic solution like this is very irritating to veins.

2. Diabetic Ketoacidosis (DKA) - type 1 DM S/E

Lack of Insulin

Decreased utilization of Glucose by

muscle fat and liver.

Increased breakdown of fat

Production of glucose by liver

Hypergylcemia

Blurred Vision

Increased fatty acids

Polyuria

Increased ketone bodies

Dehydration

Weakness
Headache

o
o
o

o
o
o

Acetone Breath

Increased Thirst

Nausea
Poor appetite

Caused by an absence or inadequate amount of insulin.

3 main causes are:
Decreased or missed dose
Infection or illness
Undiagnosed or untreated DM.
Results in disorder of carb, protein and fat metabolism.
Severity if DKA is not necessarily related to BGL.
Ketoacidosis is reflected in low serum bicarb levels and low pH.
Low PCo2 reflects respiratory compensation
Ketone bodies in blood and urine.
More common in type 1 diabetes
Rapid onset.
S/S
3 main clinical features:
Hyperglycemia

Acidosis

nausea
vomiting
abdominal pain

Increasingly
rapid
Respirations

o
o

Dehydration and electrolyte loss

Acidosis
Kussmauls Breathing
Polyuria, polydipsia
Blurred vision
Weakness and headache
Diagnostic
BS between 250-800 mg/dl
Low serum BiCarb levels
Low PH- less than 7.35 (acidosis)
Increased BUN (10-20 normal)
Prevention
For prevention of DKA related to illness
Sick day rules for managing diabetes when ill should be reviewed.
Take insulin or oral antibiotics as usual
Test BS and urine ketones q3-4hrs
Report elevated glucose levels (> 250 mg/dl) or urine ketones.
If taking insulin, may need supplemental doses or regular insulin every 3-4 hours.
If unable to follow regular meal plan, substitute soft foods (gelatin, cream soup,
custard, graham crackers) 6-8x per day.
If vomiting, diarrhea or fever persists, take liquids (regular cola, orange juice,
broth Gatorade) every to 1 hour to prevent dehydration and provide calories.
Report nausea, vomiting and diarrhea as it may lead to extreme fluid loss
May require hospitalization to avoid DKA and possibly coma if unable to retain
fluids.
Main point of sick day rules: never eliminate insulin when nausea or vomiting occur.
Treatment
TX Hypoglycemia
3 Rs Rehydrate, Reverse, Restore:
Rehydration with IV fluids:
0.9% NACL administered at rapid rate for 1-2 hours.
0.45%NS(hypotonic) may be used for pts with HTN, hyponatremia, and those at
risk for heart failure
Correct electrolyte loss
K levels < during DKA treatment. K must be infused even if plasma K level is
normal bc of this.
- K level may drop quickly as a result of rehydration and insulin treatment, Potassium
replacement must start immediately once potassium levels drop to normal.
- Frequent (initially q2-4 hours) ECGs and lab measures of K are necessary during the
first 8 hours of tx.
- Withhold only if hyperkalemia is present or if PT is not urinating.
Reverse Acidosis
Insulin stops acid buildup by inhibiting fat break down(ketone is byproduct of fat
metabolism and ketone is acidotic)
Regular Insulin will be infused at a slow continuous rate until sub q insulin
administration can be resumed.
o Usually about 12-24 hours until BS are corrected.
o Bicarb level > (we want 15-18) and until patient can eat.
Generally Bicarb infusion to correct sever acidosis is avoided during tx of DKA as it
can cause K to drop suddenly(potentially fatal)

When mixing insulin drip, you must flush insulin solution through the entire IV
infusion set and discard the first 50 ml of fluid.
We do this bc initial fluid may contain a decreased concentration of insulin since the
insulin molecules tend to adhere to the inner surface of iv sets.

3. Hyperglycemic Hyperosmolar Nonketotic Syndrome (HHNS) generally type 2

DM
o
o
o
o
o
o
o

Hyperosmolality and hyperglycemia occur due to lack of effective insulin.

Ketosis is minimal or absent
Hyperglycemia causes osmotic diuresis with loss of water and electrolytes
Hypernatremia and increased osmolality occur.
More common in type 2 diabetes- older population
Onset is slower than DKA-takes a few days
High mortality rate
S/S
Changes in mentation #1!!!
Orthostatic hypotension
Profound dehydration
Dry mucus membranes, poor skin turgor
Tachycardia
Variable neurological signs
Change in LOC, alteration of sensorium, seizures and hemiparesis
Glucosuria, Hypernatremia, and increased osmolality
Diagnostic
BG usually 600-1200 mg/dl
Osmolality exceeds 350 mOsm/kg
Increased BUN (dehydration)
Treatment
Rehydration
Same as with TX for DKA
Insulin Administration
Monitor Fluid Volume and electrolyte status
Prevention
BGSM
Diagnose and management of DM
Assess and promote self care management skills

Long Term Complications of diabetes

Macrovascular
o Accelerated atherosclerotic changes
Vessels thicken, sclerose and become occluded by plaque that adheres to the vessel wall.
Blood flow is eventually blocked.
Risk for CVA, HTN and MI
Risk factors - CAD, cerebrovascular disease, and peripheral vascular disease
S/S of PVD
Diminished peripheral pulses
Intermittent claudication (pain in butt, thigh or calf while walking)
TX
Anti-HTN and hyperlipidemia meds

Stop smoking

Microvascular
o Directly related to high blood sugar.
o Capillary basement membrane thickening
Retina and Kidneys affected
Rentinopathy, glaucoma, catarax, lens opaque, palsy eye (eye movement changes)
o 1. Diabetic retinopathy
Leading cause of blindness.
Occurs due to changes in blood vessel in eye.
Occurs in both DM 1 and 2
3 main stages
Nonproliferative
o Micro aneurisms in eye leak fluid causing swelling and forming deposits.
o Macular edema may cause Visual distortion and loss of central vision.
Preproliferative
o Increased destruction of retinal blood vessel
Proliferative (greatest threat to vision-most prone to bleeding in retina)
o Abnormal growth of new blood vessel on retina which can burst,
eventually leading to scar tissue detaching the retina
S/S
Painless Blurry vision
Floaters
Cobwebs in vision
Complete loss of vision
Diagnostic
Fluorescein angiography
o S/E of procedure may cause
Nausea during dye injection
Yellowish, fluorescent discoloration of skin & urine for 12-24hrs
Allergic reaction such as hives or itching.
Management
Primary and Secondary Prevention
o Keep BS within normal levels with intensive insulin therapy
Annual Eye Exam
o Bc may result in cataracts with lens changes, glaucoma, eye muscle palsy
Smoking cessation
Laser Coag treatment
o Laser destroys leaking blood vessel in eye
o Done outpatient, most pts can resume to normal activities by next day
o 2. Nephropathy
Increased BP in vessel of kidneys over time = nephropathy that occurs over time.
Common complication of DM.
50% of pts with End stage renal Failure are diabetic.
Pts with type 1 show initial symptoms of renal disease after 10-15 years
Those with type 2 develop renal disease within 10 years after DM diagnosis.
S/S
Positive protein in urine may be first sign of change in renal vascular pressure.
Diagnostic
BUN and Creatinine annually if dx with DM.
o Microalbuminuria > 20mg/24hours - 2 consecutive random urine test

Needs to have a 24 hours urine sample obtained and tested.

Positive results require treatment.(usually via Ace inhibitor)

Management
Control HTN
Prevent UTI
Avoid nephrotoxic meds( like antibiotics)
Low sodium and low protein diet
3. Diabetic Neuropathies
o Peripheral neuropathy, autonomic neuropathies, hypoglycemic unawareness, neuropathy and
sexual dysfunction.
o Consistently high BG affects nerves
o Capillary Basement membrane thickening and closure with de-myelinating of the nerves which
disrupts nerve conduction.
Myelin sheaths are affected-especially affects nerves of lower extremities.
o 2 most common types are sensorimotor polyneuropathy and autonomic neuropathy.
o Cranial mononueropathies-affecting cranial nerve- also occur especially in elderly.
o Sensorimotor Peripheral Neuropathy
Most commonly affects distal portions of nerves especially of the lower extremities.
Risk for foot injury
S/S
Initial paresthesias, tingling and burning sensations(especially at night)
As it progress, feet become numb.
Decrease in proprioception and decreased sensation of light touch, leading to
unsteady gait(safety issue)
May lead to foot deformity such as Charcot joint
Decreased Sweating (pseudomonas neuropathy)
Assessment
Decrease in DTRs
Management
Intensive insulin therapy and BS control
Cymbalta, an antidepressant, may treat peripheral diabetic neuropathy.
o Autonomic Neuropathies
Affects almost all organ system of body
S/S
Cardiovascular
o Slight Tachycardia
o Orthostatic hypotension
o Silent or painless MI
GI
o Bloating, nausea, vomiting (< gastric emptying)
o diabetic constipation or diarrheas(especially nocturnal)
o Wide swings in BG levels
Renal
o Urinary retention (<sensation of full bladder)
o Neurogenic bladder symptoms, UTI
o Hypoglycemic unawareness
o Sexual Dysfunction
Female - Vaginal yeast infections are common
Male erectile dysfunction

Management
o Avoid strenuous activity
o Treat symptoms
o Use elastic garments-nothing tight-will help circulation
Foot and leg Problems

Related to decreased sensory perception- loss of ability to sense pain.

Must routinely check feet and shoes that provide protection
Hyperglycemia impairs ability of specialized leukocytes to destroy bacteria
o lowers resistance to certain infections
Sift tissue injury
If progresses, can lead to gangrene and amputation.
Nails cut podiatry
Table 41-10
o Look at bare feet daily
o Use a mirror to check bottoms of feet
Check for changes in temperature
o Wash feet in warm NOT HOT water
o Dry feet well, between toes!!!!
o Do not soak feet
o Do not check temp of water with feet, use a thermometer
o Use a thin coat of skin lotion on tops and bottoms of feet NOT BETWEEN TOES
o Trim nails straight across and file edges with emery board
o Never walk barefoot- wear socks and shoes at all times
o Comfortable shoes that fit well and protect feet.
o Feel inside shoe before putting them on
o Wear shoes on beach/hot pavement
o Wear socks at night if cold
o Put feet up when sitting
o Wiggle toes and move ankles for 5 mins 2-3X/day
o Do not smoke
o Call PCP if you cut yourself ASAP