2012 annual glycemic control (adult)

8/2/2019 2012 Annual Glycemic Control (Adult)

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Glycemic Control

Annual Competency Review


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What is Diabetes

Metabolic diseases characterized by inappropriate hyperglycemia

resulting from defects in insulin secretion, insulin action, or both.

(ADA, 2003)


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Overview of Food Metabolism

Every cell in the human body

requires energy to function (24

hours/day)

The bodys primary source of

energy is glucose (blood sugar)

Glucose enters the cells with the

help ofinsulin


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FOOD SUGAR

Carbohydrates are the bodys

primary source of energy

Glucose is the end product ofcarbohydrate metabolism

Protein and fats only have a

minimal effect on blood glucose

levels.

LIVER SUGAR

In a fasting state, the liver

produces glucose from 3 sources of

stored energy

Glucogenoloysis

Glycogen (a form of glucose

stored in the liver andmuscles)

Gluconeogenesis

Amino acids (supplied from

muscle tissues)

Glycerol (supplied from fat)

Sources of Glucose


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What is InsulinInsulin is a hormone produced by the beta cells in

the pancreas.

In response to increased glucose levels, the

pancreas releases insulin into the blood stream to

help glucose enter the cells, subsequently lowering

blood glucose levels


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How Does Insulin Work

Insulin acts like a key that stimulates the cells of thebody to take up glucose (blood sugar), so that theyhave the energy to do their work.

When insulin reaches the insulin receptor sites theglucose is able to enter into the cell.

CELL WALL

Insulin Receptor Site


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The liver and the pancreas work together to control the bodys

fuel supply. After a meal, an individuals blood glucose levelrises. the pancreas releases insulin into the bloodstream tohelp the glucose enter the cells and to signal the liver to stopproducing extra glucose, subsequently lowering the bloodglucose levels. When the blood glucose level is lowered, insulinreleased from the pancreas is reduced.

NORMAL

BLOOD

SUGAR

INSULIN LIVER SUGAR

Maintaining Glucose Balance


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Classification of Diabetes

Type 1

Diabetes Type 1 is characterized by the destruction of beta

cells. Without beta cells, the body is unable to produceinsulin. Type 1 patients can get into trouble quickly when

you withhold their insulin. Even when NPO, the liver

continues to supply glucose for the cells and insulin is

required to allow the cells to utilize the insulin


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Diabetes Type 2 is characterized by insulin resistance. The

pancreas actually makes insulin, but the cells do norecognize or respond to the insulin very well, increasing

the patients insulin requirements. Eventually, the beta

cells become overworked and begin to dysfunction. At

that point the pancreas is unable to produce enough

insulin to keep blood glucose levels normal.

Type 2



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Gestational Diabetes Diabetes during pregnancy

Consists of women who develop gestational diabetes

(carbohydrate intolerance of variable severity with

the onset or first recognition during pregnancy Pregnancy is an insulin-resistant or

diabetogenic state, normally. However, there is

evidence that women who develop GDM

secrete less insulin in response to a glucose

load than women who do not develop GDM

Diabetes in the Life Cycle and Research, AADE, 2003


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SIGNS AND SYMPTOMS OF

HYPERGLYCEMIA

Polyuria (excessive urination)

Polydipsia (excessive thirst)

Polyphagia (excessive hunger) Blurred vision

Weight loss

Fatigue Muscle cramps


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Diabetic Ketoacidosis (DKA) is caused by a profound insulin deficiency. Although small amounts of insulin may be

circulating, the presence of large amounts of stress hormones (glucagon, catecholamines, cortisol, and growth hormone)

renders the insulin less effective. Carbohydrate, protein, and fat metabolism are all markedly affected. Prolonged insulin

deficiency and hormonal influences lead to the breakdown of fat in the body. Normally, ketoacids can be used by neural

and muscle tissue for energy metabolism. However the amount of ketoacids is too great. As a result, the normal

pathway becomes saturated and the pH of the blood falls.


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Signs and Symtoms of DKA

General weakness Signs of dehydration

Hypoghermia (unless an infections is present)

Acetone / fruity breath

Abdominal tenderness

Diminished breath sounds

Decreased reflexes

Blood glucose usually > 300 mg/dL

Arterial pH < 7.3

Urine and serum ketone positive


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Hyperosmolar Hyperglycemic Nonketotic Syndrome (HHNS) is characterized by high plasma osmolarity (SEVERE

dehydration volume depletion) and blood glucose in excess of 600. The presence of endogenous insulin in type 2

diabetes suppresses the lipolysis that leads to the production of ketone bodies and subsequent ketoacidosisassociated with type 1 diabetes.


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Signs and Symptoms of HHS

Symptoms of severe dehydration (orthostatic

hypotension, rapid breathing, rapid heart rate,

low B/P, and poor skin turgor)

Decreased level of consciousness

Stroke-like symptoms

Blood glucose usually > 600 mg/dL

Absence of ketosis

Arterial pH > 7.30 (no acidosis)

M b li S R


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Metabolic Stress Response

The stressresponse is the name given to the hormonal and metabolicchanges which follow injury, trauma

or illness. This is part of the systemicreaction to illness or injury which leads to hyperglycemia and

encompasses a wide range of endocrinological,immunological and hematological effects. This means you

dont have to have diabetes to be at risk for high blood sugars.

Hyperglycemia is associated with a wide range of physiologic derangements. This diagram illustrates how the

adverse effects of hyperglycemia may contribute to suboptimal patient outcomes, including high rates of

infection in hospitalized patients, disability, poor wound healing, increased mortality in some patientpopulations, and adverse health economic outcomes such as longer lengths-of-stay and increased costs.


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New Glycemic Targets

ICU: Start insulin infusion if BG>180

Goal: 140-180 mg/dL

Non- ICU:

Pre-meal:


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Optimizing Insulin Use

In order to optimize the use of insulin we should look at how the body uses

insulin and mimic the pattern of normal pancreatic secretions as close as possible.

So, lets look at how the pancreas works.


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Nutritional (Bolus) Insulin

Later, when we eat again, another burst ofinsulin is secreted from the pancreas intothe blood. The liver stops releasing storedsugar and begins to build up its stores for

later use. Nutritional intake includes: oral feeding, IVdextrose, parenteral nutrition (TPN), tubefeedings, and nutritional supplements (Ensure)

We mimic this action with rapid- or fast-acting

insulins ordered with meals


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Corrections Insulin CORRECTION INSULIN

We also use rapid- and fast-acting

insulins to correct high blood sugars

and bring them down elevated to a

normal level

Old term sliding scale

Do not holdeven if the patient

does not eat because the dose should only be enough to

reduce elevated sugars to within normal limits

If a correction dose of insulin of insulin causes hypoglycemia,notify the physician. The correction scale may be too

aggressive

Dose can be ordered as decrease bedtime dose by half or

even as Hold bedtime dose to prevent late-night

hypoglycemia events

FSBS < 60 give 1 amp of D50151-200 give 2 unit

201-250 give 4 units



>350 give 10 units, call the Dr. andrepeat FSBS in one hour


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Whats wrong with sliding scale?

The traditional sliding scale regimens do not contain basal or nutritional doses of insulin. They only consist

of pre-meal and bedtime monitoring of the patients blood glucose levels and giving a dose of insulin if the

glucose level is too high. This out-dated concept was once a standard, but a sliding scale scheme, by itself,

cannot keep blood sugars consistently in the target range.

With Sliding Scale Regimens, glycemic control is rarelyassessed. Notice that the fingersticks are taken at the

lowest levels of the day (just before meals) then the patient eats and the blood sugar immediately begins to

rise. Not only are the hyperglycemic events completely undetected, but the patient stays at elevated levels for

most of the day; putting him/her at risk for complications such as infections and poor wound healing.

Sliding Scale Regimens are usually not individualized to meet a patients specific insulin resistance level. They

tend to be one-size-fits-all regimens that do not take into account individual variability. This method is reactive

instead ofproactive (treats hyperglycemia but doesnt prevent it) and is NOT recommended for use as

monotherapy for greater than 48 hours. Clinical evidence indicates that Sliding Scale Insulin as a primary

therapy is ineffective and potentially dangerous and frequently causes a harmful rollercoaster effect.


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Nutritional and Correction insulin doses, should be ordered using the

SAME type of insulin and should be given together, in the same syringe, atthe same time to prevent unnecessary sticks (usually given just prior toeating)

Nutritional insulin is the only insulin that is dependent upon whether the

patient eats or not Basal insulin should always be given according to the order (even if NPO or

if FSBS is low)

Correction insulin should always be given (even if NPO)

A physicians order required for holding insulin

Basal/Bolus Concepts


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NEUROGENIC SYMPTOMS NEUROGLYCOPENIC SYMPTOMS

Adrenergic

Heart pounding

Nervousness and anxiety

Shakiness and tremulousness

Cholinergic

Hunger

Sweating

Tingling

Behavioral changes

Brain damage

Confusion

Death

Difficulty thinking / slurred speech

Emotional liability

Fatigue

Loss of consciousness Seizures

Weakness / uncoordination

Occurs in early or mild hypoglycemia

Patient is ABLE to self-treat

Response to the increase in epinephrine

Occurs in late or severe hypoglycemia

Patient is UNABLE to self-treat

Response to the decrease in glucose to the brain


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Causes of Hypoglycemia

Too much medication Insulin given at an inappropriate time

Lack of coordination between

transportation and nursing.

Delaying of food lack of coordination between dietary and nursing leads

to mistiming of insulin dosage with respect to food

Instruct patient to inform staff when ordering or

receiving food. Not eating after taking diabetes medication


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Everyone knows that too much insulin can lead to hypoglycemia butwe need to also remember that over treating hypoglycemia can be

just as dangerous, causing rebound hyperglycemia and the bloodsugar rollercoaster effect.


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Caution should betaken with multiple,consecutive dosing

of Regular insulin

Onset: - 1 hourPeak: 1-2 hours

Duration : 5-8 hour



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Delayed response and late snowballing from repeated insulin doses mayoccur among patients with poor perfusion of subcutaneous sites. Insulinbuilds up in the tissues and is absorbed simultaneously once perfusion isrestored leading to overdosing of insulin and hypoglycemia..

Hypoalbuminemia

Edema

Hypotension

Pressors

Renal failure or renal insufficiency also has a serious impact on circulatinginsulin levels by reducing insulin clearance and allowing insulin toaccumulate in the circulation



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Be Aware of Hypoglycemic Unawareness

The early signs of hypoglycemia occur due to a response to the increase in epinephrine (adrenaline)

and can be used as a warning signal for prompt treatment. However, over the course of diabetes, or

following repeated episodes of hypoglycemia, patients can develop a delayed or diminished response

to epinephrine resulting in reduced hypoglycemic symptom awareness. This decreases response time

before severe symptoms appear and places patient at risk for unrecognized hypoglycemia 24 to 48

hours after an episode of hypoglycemia.


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False Lows

Sometimes a person may have symptoms of lowblood sugar levels, but the blood sugar levels are

not actually low. This is called a false reaction.The hormone adrenaline is not just releasedwhen blood sugar drops too lowits alsoreleased when blood sugar levels fall tooquickly.

There is no need to treat a false reaction. Justhave the patient lie down for about 10 minutesand the symptoms will subside and continue tomonitor the patients blood sugar and symptomsuntil they are stabilized.



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Treating Hypoglycemia

Use the 15/15 Rule or Fast 15 Give 15g. of fast-acting carb and wait 15 minutes before retaking FSBS--

-repeat if needed---if a meal is not available within 30 to 60 minutes,give the patient a snack with protein (P/B and crackers, cheese andcrackers, meat sandwich, glass of milk,etc) to prevent hypoglycemiafrom reoccurring

15 grams carbs or ONE carbohydrate choice 3 glucose tablets

4 oz of non-diet cola

4 oz of fruit juice DO NOT ADD SUGAR

an amp of D50 (always follow physicians order)

Limit treatment to 15 grams at a time.

Over-treating hypoglycemia causes the

roller coaster affect.

15 grams of carbs elevates the blood sugar 30-40 points and is usuallysufficient for most events


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Able to Eat

Adult Hypoglycemia orders

Provide aFAST 15


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Unable to Eat

IV Present


Its Time

for D50


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Unable to Eat

No IV Present


IM

Glucagon


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HypoglycemiaFinish What You Started

V/S + Neuro Check 15 minutesafter each treatment or until stable

Notify MD

Document: interventions, patient response,and MD notification

If FSBS < 40 and the patient is asymptomatic, redo thetest at another site (venous specimen preferred)

Identify Patient as High Risk for Hypoglycemia for next

24 hours


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Close Monitoring

FSBSs must be retaken if the correction insulinis not administered within one hour of FSBS

FSBSs should be repeated if the glucometer

reads "HI" (>600) or "LO" (


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Patient Education: Walk & Talk

Diabetes Dia-log

Heres your basal insulin

Mrs. Jones. Its a long-acting insulin that covers

your fasting insulinrequirements.

I need you to practicedrawing it up and giving it

to yourself.

Ill be right here if you

need me.


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The Power of One

Become A Glycemic Control Advocate

Promote best practicesClarify any orders that you feel areinaccurate or inappropriate

Initiate treatment changes to coincide withstatus changes or treatment failureCommunicate to the members of yourhealthcare teamListen to the patient---they usually know

more about controlling their own glucose thanwe do. Do not ignore their comments.Instead, utilize them to improve the patients

care

2012 annual glycemic control (adult)

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