Diabetes Mellitus (Part II)TreatmentAcute ComplicationsChronic ComplicationsPatient Teaching

Treatment

Drug Therapy: InsulinOral Agents

Nutritional TherapyExercise Pancreas Transplant

Treatment

•The goal of any treatment for Diabetes:Reduce symptomsPromote well-beingPrevent acute complicationsPrevent 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 insulinBlood Glucose Levels can be controlled by

diet & exercise aloneMay 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:

OnsetPeak 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 InsulinRapid-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

HumalogNovolog

Short acting Regular Insulin: Onset = 30-60 minutes

“Regular”• Should be injected 20-30 minutes before a meal

Intermediate Acting Insulin

•NPH InsulinOnset 2-4 hoursPeaks 4-12 hoursDuration - 16-24 hoursGenerally 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 levelLantusLevemir

•No PeakRisk for hypoglycemia greatly reduced

Long Acting Insulin (cont’d)

•Lantus and/or Levemir:Given once in the morning or at bedtimeCannot be mixed (in syringe) with other

insulinsCannot 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 RegularNovolog 70/30 mix

70% NPH – 30% Novolog RegularHumulin 50/50 mixHumalog 75/25

Administration of Insulin

•Insulin is inactivated by gastric juices – cannot be taken orallyInjectionInsulin PenInsulin PumpInhaled 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 ReactionsLocal; itching, burning usually due to

additivesTrue insulin allergy is rare, but can be

anaphylactic •Lipodystrophy: Atrophy of subcutaneous

tissuePrevented by rotation of sitesMay result in poor absorption of insulin

• Somogyi Effect • Dawn Phenomenon

Somogyi Effect •Somogyi Effect is a ‘rebound’ effect

Overdose of insulin induces hypoglycemiaUsually 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 peako 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 resistance2. Decreased insulin production3. 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 hypoglycemiao 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 oMetformin (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 intestineoAcarbose (Precose)oMiglitol (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 tissueso Pioglitazone (Actos)oRosiglitazone (Avandia)

• Most effective for people with insulin resistanceDo 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. Good Metabolic Control2. Maintain blood glucose levels at or near normal3. Achieve lipid profiles and BP levels 4. Modify Lifestyle changes as appropriate 5. 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 othersCultureTeach the person who does the cookingCaloric 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 levelsCan also decrease triglycerides, LDL

cholesterolCan increase HDLCan reduce blood pressureCan 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

stressCounterregulatory 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 self-

management decisions regardingDietExerciseMedications

•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 aloneCan 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

Acute Complications of Diabetes MellitusHypoglycemiaDiabetic 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:ConfusionIrritabililtyDiaphoresisTremorsHungerWeaknessVisual 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 HypoglycemiaConscious Patient Unconscious Patient

• Give the patient 15-20 grams of quick acting carbohydrate4-6 oz Regular soda8-10 Candies4-6 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

Hypoglycemia is an emergency and needs to be treated immediately

Diabetic Ketoacidosis (DKA)• Also known as Diabetic Coma• Caused by: A profound deficiency of insulin

and characterized by:hyperglycemiaketosisacidosis 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 TurgorDry mucous membranesTachycardiaOrthostatic HypotensionLethargy, weakness

•Severe Dehydration:Skin dry & looseEyeballs 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 breathSweet, fruity breath odorKetonuria

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 DiabeticsSeen 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 InsulinContinual 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

Chronic Complications of Diabetes Mellitus

Macrovascular/Microvascular ComplicationsDiabetic RetinopathyNephropathyNeuropathyComplications of Feet & Lower ExtremitiesIntegumentary Complications

Complications: Diabetes MellitusMacrovascular 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 diseaseGenetic 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 EyeKidneyNerves

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 levelsTight 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

neuropathyOccurs with equal frequency in Type 1 &

Type 2•Can lead to loss of (protective) sensation

in lower extremitiesIncreases risk of complications that result

in amputation of lower limbsoMore than 60% of non-traumatic amputations

are diabetics

Diabetic Neuropathy (cont’d)Sensory Neuropathy Autonomic Neuropathy

• Distal symmetric neuropathy Affects hands and/or feet

bilaterallyLoss of Sensation: Can be

complete or partial loss of sensation

Pain: burning, crushingAbnormal sensationsParesthesias Tingling,

burning or itching

• 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 Repetitive injuryo Stepping on foreign objects when barefooto Ill-fitting footwear

2. Peripheral Arterial Disease Causes a reduction in blood flow to lower

extremities Wounds take longer to healo Increases the risk for infection

Diabetic Foot Ulcers

Integumentary

•Diabetic DermatopathyRed-brown, flat-topped papules

•Necrobiosis lipoidica diabeticorumMay 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

•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