Diabetes Mellitus (Part II)
Treatment
Acute Complications
Chronic Complications
Patient Teaching
Drug Therapy:
Insulin
Oral Agents
Nutritional Therapy
Exercise
Pancreas Transplant
Treatment
• The goal of any treatment for Diabetes:
Reduce symptoms
Promote well-being
Prevent acute complications
Prevent or delay the onset and progression of
long-term complications
• Above goals can only be met by patient
maintaining blood glucose levels at or near
normal!
Insulin Therapy (Exogenous Insulin)
• Patients with Type 1 Diabetes always require
Exogenous insulin (insulin from a source outside
the body)
• Type 2 Diabetics may not need any insulin
Blood Glucose Levels can be controlled by diet &
exercise alone
May need insulin eventually due to chronic and
progressive nature of the disease
Types of Insulin
•
•
•
•
No longer made from beef or pork pancreas
Only human insulin is used today
Human insulin made from bacteria or yeast cells
Insulins differ in regard to:
Onset
Peak action
Duration
• Characterized according to the amount of time
they need to take effect
• Read the label carefully
See Insulin Comparison Chart
Insulin Therapy
• Specific properties of each type of insulin are
matched with the patient’s diet and activity
• Can range from one injection per day to several
injections of various types of insulin
• Most closely resembles endogenous insulin
production:
Basal-bolus regimen
• The regimen chosen should be mutually selected by
the patient and the HCP
• Criteria for selection are based on the desired and
feasible levels of glycemic control and the patient’s
lifestyle
Fast/Rapid Acting Insulin
Rapid-acting
• Mealtime Insulin – Bolus
• Used to control post-meal blood glucose levels
• Rapid Acting Insulin: Onset = 15 minutes
• Should be given 15 minutes before a meal
Humalog
Novolog
Short acting Regular Insulin: Onset = 30-60
minutes
 “Regular”
• Should be injected 20-30 minutes before a meal
Intermediate Acting Insulin
• NPH Insulin
Onset 2-4 hours
Peaks 4-12 hours
Duration - 16-24 hours
Generally given twice a day before meals
Long Acting (Basal) Background
Insulin
• Long-acting/basal (background) insulin to
control blood glucose levels between meals and
overnight
• Provides 24 hour steady and continual
background insulin to keep blood glucose levels
at a constant or controlled level
Lantus
Levemir
• No Peak
Risk for hypoglycemia greatly reduced
Long Acting Insulin (cont’d)
• Lantus and/or Levemir:
Given once in the morning or at bedtime
Cannot be mixed (in syringe) with other insulins
Cannot be pre-filled
Combination Insulin
• Insulins can generally be mixed in the same
syringe
• Some Insulins Come Pre-mixed
Novolin 70/30 mix
70% NPH – 30% Novolin Regular
Novolog 70/30 mix
70% NPH – 30% Novolog Regular
Humulin 50/50 mix
Humalog 75/25
Administration of Insulin
• Insulin is inactivated by gastric juices – cannot
be taken orally
Injection
Insulin Pen
Insulin Pump
Inhaled Insulin
Administration of Insulin:
Subcutaneous Injection
• Injection
• Gently rotate insulin in hands to warm
• Mixing Insulins for Injection
Lantus/Levemir cannot be mixed
Don’t mix insulins from different manufacturers
• Regular/NPH Insulin mix:
Draw up Regular insulin first, then add NPH
Subcutaneous Insulin Injection
(cont’d)
• Absorption of Insulin varies according to the
injection site used
Slower
Fastest
Insulin Administration (cont’d)
The Insulin Pen
Compact & Portable
Looks less like a syringe
Handy, Calibrated
Pre-filled with Insulin
* Change needle for each
use
Insulin Pump
Can be worn on belt or clothing
Tubing inserted into
subcutaneous tissue in
abdomen
Site must be changed every 3
days
Can deliver basal rate, short
and long acting insulin
User programs according to
exercise, diet, etc. )
Insulin Pump
The MiniMed Paradigm
insulin pump (A) delivers
insulin into a cannula (B)
that sits under the skin.
Continuous glucose
monitoring occurs through
a tiny sensor (C) inserted
under the skin. Sensor data
are sent continuously to the
insulin pump through
wireless technology.
Courtesy of Medtronic
Diabetes.
Inhaled Insulin (Exubera)
• Alternative to injectable insulin
• Rapid Acting; replaces short-acting ‘coverage’
insulins
• Inhaled before meals
• Usually added to longer acting insulins for type
1 diabetics
•Type 2 diabetics: Alone or with any
combination of prescribed insulins
•Contraindications:




Smoker
Quit smoking within last 6 months
Asthma
PFTs before prescribed
Problems with Insulin Therapy
• Allergic Reactions
Local; itching, burning usually due to additives
True insulin allergy is rare, but can be
anaphylactic
• Lipodystrophy: Atrophy of subcutaneous tissue
Prevented by rotation of sites
May result in poor absorption of insulin
• Somogyi Effect
• Dawn Phenomenon
Somogyi Effect
• Somogyi Effect is a ‘rebound’ effect
Overdose of insulin induces hypoglycemia
Usually occurs during hours of sleep
• Normal/elevated blood glucose at bedtime, a
decrease at 2-3 am  hypoglycemic levels, and
increase caused by the production of
counterregulatory hormones released,
producing rebound hyperglycemia
• The danger  the morning BGL can be high in
response to the counterregulatory hormones and
the MD may increase the insulin dose
Dawn Phenomenon
• Similar to Somogyi
• Relatively normal glucose until about 3am then
the glucose level begins to rise.
• Hyperglycemia is present on awakening in the
morning due to the release of counterregulatory
hormones in the pre-dawn hours.
Possibly caused by growth hormone
Affects all diabetics at one time or another, more
severe when growth hormone is at it’s peak
o Adolescence and young adulthood
Careful monitoring of insulin, snacks and BGLs
Oral Drug Therapy
Oral Agents are NOT oral forms of insulin
• Oral agents work to improve the
mechanisms by which insulin and glucose are
produced and used by the body – they work on
the 3 defects of type 2 diabetes:
1. Insulin resistance
2. Decreased insulin production
3. Increased hepatic glucose production
•
May be taken in combination with each other
or with insulin to achieve BGL targets
Oral Hypoglycemic Agents
• Sulfonylureas: increases insulin production
from the pancreas
• Drug of choice in Type 2 Diabetes because of
decreased chance of hypoglycemia
o glipizide (Glucotrol, Glucatrol XL)
o glyburide (Micronase, DiaBeta, Glynase)
o glimiperide (Amaryl)
Interacts with oral anticoagulants
Oral Hypoglycemics (cont’d)
• Biguanides: Primary action is to reduce
glucose production by the liver
o Metformin (Glucophage)
• Can be used alone or with other oral agents or
insulin to treat Type 2 Diabetes
• Also used in prediabetics to prevent type 2
diabetes
• Does not promote weight gain
 Cannot be taken with contrast dye!
Oral Hypoglycemic Agents (cont’d)
• a -Glucosidase Inhibitors: (starch blockers)
work by slowing down absorption of
carbohydrates in the small intestine
o Acarbose (Precose)
o Miglitol (Glyset)
• Taken with first bite of each meal
• Most effective in lowering post-prandial BGLs
Oral Hypoglycemic Agents (cont’d)
• Thiazolidinediones: a/k/a Insulin Sensitizers,
work by improving insulin sensitivity, transport and
utilization at target tissues
o Pioglitazone (Actos)
o Rosiglitazone (Avandia)
• Most effective for people with insulin resistance
Do not cause hypoglycemia because they don’t
increase insulin production
Can cause edema – do not use in patients with heart
failure
Diabetes Treatment
The Priority Nursing Considerations for any
diabetic patient on Insulin or oral Hypoglycemic
agents is
Monitor/prevent Hypoglycemia
Hypoglycemia is an emergency and needs to be
treated immediately
Nutritional Therapy
Type 1 Diabetes Mellitus
Type 2 Diabetes Mellitus
• Meal planning based on
patient’s usual food intake
• Balance with insulin and
exercise programs
• Plan is developed with the
person’s eating habits and
activity pattern in mind
• Emphasis is based on
achieving glucose, lipid and
blood pressure goals
• Reduce total fat, simple
sugars, carbohydrates
• Space Meals
• Weight loss of even 5 – 7% can
improve glycemic control
Diabetes: Nutritional Therapy
• The Cornerstone of Care for the patient with
Diabetes
The Goal (according to the ADA) is to assist people
with diabetes to make good food choices and
maintain healthy exercise habits that lead to:
1.
2.
3.
4.
5.

Good Metabolic Control
Maintain blood glucose levels at or near normal
Achieve lipid profiles and BP levels
Modify Lifestyle changes as appropriate
Improve health through healthy food choices and
physical activity
Must address individual nutritional needs, personal
and cultural preferences and respect the individual’s
willingness to change
Patient Teaching (Nutritional Tx)
• Nurses often assume responsibilities of teaching
• Ideally: Diabetic teacher or interdisciplinary
diabetes care team
• Include
Patient’s family and significant others
Culture
Teach the person who does the cooking
Caloric intake
Patient Teaching: Exercise Therapy
• Regular, consistent exercise is an essential part
of diabetes and prediabetes management
Exercise increases insulin receptor sites in the
tissue and has a direct effect on lowering blood
glucose levels
Can also decrease triglycerides, LDL cholesterol
Can increase HDL
Can reduce blood pressure
Can improve circulation
Exercise Therapy (cont’d)
• Exercise can lower BGLs to dangerously low levels
Small carbohydrate snacks can be taken 1 hour before,
1 hour after exercise
Patient should exercise and carry a fast acting
carbohydrate
• Exercise can also raise BGLs
The body sometimes perceives the exercise as a stress
Counterregulatory hormones released, raising BGLs
• BGLs should be monitored before, during & after
when beginning an exercise regimen, especially if
the patient formerly led a sedentary lifestyle
Monitoring Blood Glucose Levels
• Self-Monitoring of Blood Glucose (SMBG) = a
cornerstone of diabetes management
• SMBG enables the patient to make selfmanagement decisions regarding
Diet
Exercise
Medications
• Important for detecting episodes of
hyperglycemia and hypoglycemia
• Teaching SMBG is an important nursing
responsibility
Pancreatic Transplant
• Treatment option for Type 1 Diabetics with
poorly controlled BGLs
Rare, usually not done alone
Can be done following kidney transplant to protect
the new kidney from further damage from high
BGLs
Pancreas transplant only partially successful in
reversing long-term damage
Patient must take life-long immunosuppressants
Hypoglycemia
Diabetic Ketoacidosis (DKA)
Hyperosmolar Hyperglycemic Syndrome (HHS)
Hypoglycemia
• Hypoglycemia occurs when there is too much
insulin in proportion to available glucose in the
blood . BGL drops to <70
Common Manifestations of hypoglycemia:
Confusion
Irritabililty
Diaphoresis
Tremors
Hunger
Weakness
Visual Disturbances
Hypoglycemia
• The brain requires a constant supply of glucose
in sufficient quantities to function properly,
hypoglycemia can affect mental function
• Manifestations of hypoglycemia can mimic
alcohol intoxication
• Untreated hypoglycemia can progress to loss of
consciousness, seizures, coma, death
Low Blood Glucose Levels
• Hypoglycemia may also result if high glucose
levels are treated too aggressively and brought
down too quickly
• It is important to ascertain why the BGL
dropped
Treatment of Hypoglycemia
Conscious Patient
Unconscious Patient
Hypoglycemia is an emergency and needs to be treated immediately
• Give the patient 15-20 grams
of quick acting carbohydrate
 4-6 oz Regular soda
 8-10 Candies
 4-6 oz Orange Juice
• Repeat in 15 minutes if no
improvement
• Longer acting carbohydrate
 Crackers with peanut butter
or cheese
 Immediate notification of
health care provider especially
if symptoms do not subside
• Subcutaneous or IM injection
of 1 mg Glucagon
• IV administration of 50 mls of
50% Glucose
Diabetic Ketoacidosis (DKA)
• Also known as Diabetic Coma
• Caused by: A profound deficiency of insulin and
characterized by:
hyperglycemia
ketosis
acidosis
dehydration
• Most likely to occur in Type 1 Diabetics, but
sometimes occurs in Type 2 Diabetics during
conditions of severe illness and/or stress
Diabetic Ketoacidosis (cont’d)
• Ketones are the acidic by-products of fat
metabolism
• Ketosis (presence of ketones in the blood) alters
the Ph balance causing metabolic acidosis
• Ketonuria begins – ketone bodies are excreted in
the urine
• The kidneys use more water to eliminate the ketones
– causes dehydration
• The existing insulin deficiency causes proteins to
break down and stimulates production of glucose
(in the liver) leading to worsening hyperglycemia
Diabetic Ketoacidosis (cont’d)
• The rise in glucose levels and lack of insulin make
the blood glucose levels rise even further
• With cell death, potassium is released from cell
into the bloodstream -> hyperkalemia
• Kidneys continue to excrete ketones – leading to a
severe depletion of Potassium & other electrolytes
Diabetic Ketoacidosis
• Acidosis causes nausea & vomiting which results
in severe hypovolemia, possibly shock
• Renal failure results from hypovolemic shock
(which causes retention of ketones & glucose
and the acidosis progresses)
Diabetes Ketoacidosis (cont’d)
• Result: Patient becomes comatose as the result
of dehydration, electrolyte imbalance and
acidosis
 Coma
 Cardiac irregularities (due to hyperkalemia)
 Renal insufficiency
 Eventual death
DKA: Clinical Manifestations
• Dehydration- Early signs include:
Poor Skin Turgor
Dry mucous membranes
Tachycardia
Orthostatic Hypotension
Lethargy, weakness
• Severe Dehydration:
Skin dry & loose
Eyeballs soft, sunken
DKA: Clinical Manifestations (cont’d)
• Abdominal Pain accompanied by anorexia &
vomiting
• Kussmaul respirations (rapid, deep
breathing associated with dyspnea)
The body is attempting to reverse the metabolic
acidosis through exhalation of excess Co2.
Acetone noted on the breath
Sweet, fruity breath odor
Ketonuria
Management
• Correct dehydration
• Correct electrolyte loss
• Acidosis
Hyperosmolar Hyperglycemic
Syndrome
• Formerly known as Hyperosmolar
Hyperglycemic Non-Ketoacidosis (HHNK)
• HHS is a life-threatening syndrome that can
occur when the person is able to produce enough
insulin to prevent DKA (and ketoacidosis) but
not enough to prevent severe hyperglycemia,
osmotic diuresis and extracellular fluid
depletion.
DKA vs. HHS (HHNK)
• DKA usually Type 1 Diabetics
• HHNK usually Type 2 Diabetics
Seen more often in elderly with pre-existing
cardiac or renal problems
Usually patient can produce enough insulin to
avoid ketoacidosis but not enough to prevent
profound hyperglycemia, dehydration and
hyperosmolality
• Risk factors
• Clinical picture
Treatment DKA/HHS
• IV Fluids
• IV Insulin
Rapid Acting Insulin
Continual drip
• Electrolyte Replacement
• Assessment of Mental Status
Safety
•
•
•
•
•
I & O’s
Central Venous Pressure Monitoring (if indicated)
Blood Glucose Levels
ECG Monitoring
Cardiovascular and Respiratory Status
Macrovascular/Microvascular Complications
Diabetic Retinopathy
Nephropathy
Neuropathy
Complications of Feet & Lower Extremities
Integumentary Complications
Complications: Diabetes Mellitus
Macrovascular
Microvascular
• Diseases of the large &
medium size blood vessels
• Exact cause unknown –
related to the altered lipid
metabolism -> atherosclerotic
plaque formation
 Cerebrovascular
 Coronary Artery
 Peripheral Vascular
• Diseases resulting from the
thickening of the vessel
membranes in the capillaries
and arterioles in response to
conditions of chronic
hyperglycemia
(Microangiopathy)
 Diabetic Retinopathy
 Diabetic Nephropathy
 Dermopathy
o Diabetic Foot Ulcers
Macrovascular Complications
• Adults with Diabetes have 2-4 x increased risk
of cerebrovascular and cardiovascular disease
Genetic risk not modifiable
Other risk factors can be modified (obesity,
smoking, HTN, high fat intake, sedentary lifestyle)
Blood Pressure Control significantly reduces the
risk of microvascular complications
Eye
Kidney
Nerves
Diabetic Retinopathy
• The process of microvascular damage to the
retina as the result of chronic hyperglycemia in
patients with diabetes
• Subject to many visual complications
• Assessment /Dx
• Treatment:
Photocoagulation (Laser) destroys the ischemic
area producing the growth factors
Vitrectomy: aspiration of fluid & fibers from the
inside of the eye
Diabetic Nephropathy
• Definition: A microvascular complication
associated with damage to the small blood
vessels that supply the glomeruli of the kidney.
• Leading cause of End Stage Renal Disease
(ESRD) in the U.S.
• Same risk, type 1 or type 2 Diabetics
Diabetic Nephropathy (cont’d)
• The risk for kidney disease in diabetics can be
significantly reduced when blood glucose levels
are closely controlled to near-normal levels
Tight blood glucose control critical
• ACE inhibitor (Angiotensin Converting
Enzyme) medications sometimes prescribed for
diabetics because of the protective effect they
have on the kidneys
Diabetic Neuropathy
• 60-70% of diabetics have some form of
neuropathy
Occurs with equal frequency in Type 1 & Type 2
• Can lead to loss of (protective) sensation in
lower extremities
Increases risk of complications that result in
amputation of lower limbs
o More than 60% of non-traumatic amputations are
diabetics
Diabetic Neuropathy (cont’d)
Sensory Neuropathy
• Distal symmetric neuropathy
 Affects hands and/or feet
bilaterally
 Loss of Sensation: Can be
complete or partial loss of
sensation
 Pain: burning, crushing
 Abnormal sensations
 Paresthesias Tingling,
burning or itching
Autonomic Neuropathy
• Autonomic Neuropathy: Can
affect all body systems and lead
to hypoglycemic unawareness,
constipation or diarrhea or
urinary retention
 Gastroparesis
 Cardiovascular abnormalities
• Sexual dysfunction often the
first manifestation
 Decreased libido
 Erectile dysfunction
 Vaginal infection
• Neurogenic Bladder
 Urinary retention
Diabetic Neuropathy
Management
• diet high in sodium
• avoid agents that stimulate ANS
• wear elastic garments
• frequent monitoring blood glucose
• low-fat diet
• increase gastric motility
• anti-diarrhea medications
• high fiber diet/hydration
Diabetic Neuropathy
Complications of the Feet & Lower
Extremities
• Foot complications = the most common cause of
hospitalization of the person with diabetes
• “Diabetic Foot” is the result of both
microvascular and macrovascular disease
processes which frequently leads to:
 Injury
 Serious Infection (Cellulitis)
 Amputation
Feet & Lower Extremities (cont’d)
• Multifactoral Process: The Two Major Causes of
Diabetic Foot Ulcers are:
1. Sensory neuropathy causes Loss of Protective
Sensation (LOPS)
 Patient is unaware of injury
o
o
o
Repetitive injury
Stepping on foreign objects when barefoot
Ill-fitting footwear
2. Peripheral Arterial Disease
 Causes a reduction in blood flow to lower extremities
 Wounds take longer to heal
o
Increases the risk for infection
Diabetic Foot Ulcers
Integumentary
• Diabetic Dermatopathy
Red-brown, flat-topped papules
• Necrobiosis lipoidica diabeticorum
May appear before other clinical signs &
symptoms
Foot /Leg Problems
Risk factors
• Diabetes for more than 10 years
• Older than 40 years
• History of smoking
• Decreased peripheral pulses
• Decreased sensation
• History of previous foot ulcers
Foot /Leg Problems
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•
•
•
•
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Daily assessment of the feet
Examine feet at least once a year
Assess for neuropathy
Proper bathing/drying/lubricating
Closed - toed shoes/socks
Protect feet from hot/cold