Diabetes Mellitus

1
Diabetes Mellitus
2
Physiology of Energy Metabolism

• All body cells use glucose for energy.
• To maintain this constant source of energy, blood
  glucose levels must be kept between 3.3-6.1
  mmol/L.
• Several hormones, help to maintain this level
  between 3.3-6.1mmol/L, include insulin, glucagon.
• The insulin and the glucagon together maintain a
  constant level of glucose in the blood by
  stimulating the release of glucose from the
  liver. The glucagon is released when blood
  glucose levels decreased (e.g. between meals and
  over the night) and stimulate the liver to
  release stored glucose.

3
Insulin

• Diabetes is a disease which deals with insulin.
• A healthy pancreas releases 40-50 units of
  insulin daily, still keeping several hundred
  units available in storage to be released if the
  blood glucose levels rise.
• When insulin enters the bloodstream, it binds to
  insulin receptors on the membranes of the liver,
  muscle, and fat cells. In these cells, insulin
  encourages glucose uptake by causing a shift of
  another insulin sensitive glucose transporter,
  GLUT 4, to the surface of cells.

4
Pathophysiology of Diabetes Mellitus

• Diabetes mellitus is not a single disease but a
  complex syndrome characterized by hyperglycemia
  resulting from altered carbohydrate, fat, and
  protein metabolism.
• This altered metabolism is secondary to insulin
  insufficiency, insufficient insulin activity, or
  both.
• Because of the altered fuel metabolism, diabetes
  is characterized by vascular and neurologic
  changes throughout the body.
• Absence of insulin or ineffective insulin
  activity prevents glucose from entering liver,
  muscle and fat cells

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Pathophysiologyof Diabetes Mellitus

• As the blood glucose level approaches 10mmol/L,
  the ability of the kidney to reabsorb glucose is
  surpassed, and glucose is excreted into the
  urine.
• Because it is an osmotic diuretic, glucose causes
  the osmosis of large amounts of water and
  electrolytes into the tubules, causing frequent
  urination in large quantities (polyuria), notably
  at night (nocturia). Dehydration, hunger, and
  fatigue follow.

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Classical manifestations of diabetes

• Polyuria increased urination
• Polydispia increased thirst, which occurs as a
  result of excess loss of fluid associated with
  osmotic diuresis.
• Polyphagia increased appetite which results
  from the catabolic state induced by insulin
  deficiency

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Types of diabetes

• Type I
• Type II
• Gestational diabetes

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Type I

• This is characterized by the destruction of the
  pancreatic beta cells and early onset
• The destruction of the beta cells results in
  decreased insulin production, unchecked glucose
  production by the liver and fasting
  hyperglycemia.
• Glucose derived from food is not stored in the
  liver but remains in the blood stream and
  contributes to postprandial (after meals)
  hyperglycemia
• .

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SS

• Increased thirst
• Frequent urination
• Fatigue
• Excessive weight loss
• Nausea and vomiting
• Having dry, itchy skin
• Feeling of numbness and tingling in the feet
• Blurry eyesight
• Constant hunger
• Abdominal pain if DKA (Diabetic Ketoacidosis)
  have occurred

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Type II

• This the most common form of diabetes, often
  associated with older age, obesity, family
  history of diabetes e.t.c.
• In type 2 diabetes, the pancreas is usually
  producing enough insulin, but for unknown reasons
  the body cannot use the insulin effectively, a
  condition called insulin resistance. After
  several years, insulin production decreases. So
  thus glucose builds up in the blood and the body
  cannot make efficient use of its main source of
  fuel
• These patients are not prone to the development
  of DKA.

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S S

• Fatigue
• Frequent urination
• Increased thirst and hunger
• Blurred vision

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Gestational diabetes

• Gestational diabetes is a type of diabetes that
  occurs in non-diabetic women during pregnancy. It
  is any degree of glucose intolerance with its
  onset during pregnancy or late in pregnancy. This
  form of diabetes usually disappears after the
  birth of the baby.

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Risk factors of gestational diabetes

• Over the age of 30
• Obesity
• Family history of diabetes
• Having previously given birth to a very large
  child (over 9 pounds, 14 ounces), having
  previously given birth to a stillborn child or a
  child with a birth defect
• Having too much amniotic fluid
• Having gestational diabetes in a previous
  pregnancy
• Having high blood pressure

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S S

• Generally, gestational diabetes may not cause any
  symptoms however, the woman may experience
• Excessive weight gain,
• Excessive hunger or thirst,
• Excessive urination
• Recurrent vaginal infections

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Diagnosis of diabetes

• DM is indicated by typical SS and confirmed by
  measurement of plasma glucose.
• Fasting plasma glucose (FPG) measurement after
  an 8-12h fast.
• Oral glucose tolerance testing (OGTT) 2h after
  ingestion of a concentrated glucose solution.
  OGTT is more sensitive for Dx DM and impaired
  tolerance but is more expansive and less
  convenient and reproducible than FPG. It is
  rarely used routinely, except for Dx of
  gestational DM.
• HbA1c testing for glycosylated hemoglobin.
  HbA1c levels reflect glucose control over the
  preceding 2-3 months. HbA1c is not considered as
  reliable as FPG or OGTT testing for Dx DM and
  used mainly for monitoring DM control.

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Diagnosis of diabetes (cont)

• Diagnostic criteria for DM and impaired glucose
  regulation

Test Normal Impaired glucose regulation Diabetes
CBG 3.3-6.1mmol/L
FPG lt5.6mmol/L 5.6-6.9mmol/L gt7.0mmol/L
OGTT lt7.7mmol/L 7.7-11.0mmol/L gt11.1mmol/L
HbA1c 3-6 gt7
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HbA1c

• Glucose sticks to the haemoglobin to make a
  glycosylated haemoglobin molecule, called
  haemoglobin A1c or HbA1c.
• The more glucose in the blood, the more
  haemoglobin A1c or HbA1c will be present in the
  blood.
• Red cells live 120 days before they are replaced.
  By measuring the HbA1C it can tell you how high
  your blood glucose has been on average over the
  last 8-12 weeks. A normal non-diabetic HbA1C is
  3.5-5.5. In diabetes about 6.5 is good.
• The HbA1C test is currently one of the best ways
  to check diabetes is under control the HbA1C is
  not the same as the glucose level.

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• Management of Diabetes

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Good Diabetes Management

• Regular Blood Glucose Monitoring

• Healthy Nutrition 

Regular Exercise
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Nutrition

• There isn't one "diabetes diet."
•  The amount of food you can eat daily depends on
  
• Age
• -Body size
• -Activity level
• -Gender
• -Pregnancy or breastfeeding
• Meal plan should be individualized for each
  client
• With the help from a dietician, a diet is planned
  based on the recommended amount of calories,
  protein, carbohydrates, and fats.
• A meal plan is a guide that tells you what kinds
  of food you can choose at meals and snack time
  and how much to have. For most people with
  diabetes (and those without, too), a healthy diet
  consists of 40 to 60 of calories from
  carbohydrates, 20 from protein and 30 or less
  from fat.

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Nutrition (cont)

• 1500-1800 calorie is the ideal of amount that
  diabetes diet should have. This should include
  simple and healthy foods like whole grains,
  vegetables, fruits, low fat meats, non-fatty
  dairy products and fish but avoid foods like
  pastries, candy bars and pies.
• Note
• This does not include people, like pregnant
  women, those with eating disorder and children
  under 16 should seek medical advice before
  modifying their diet to adopt 1500-1800 calorie
  diabetes diet.
• Carbohydrates (50-55 of energy), like whole
  grains, fruits, vegetables, milk, high fiber
  foods.
• Proteins (15-20 of energy).
• Fat (lt30 of energy)
• Example of 1500 calorie diabetes diet
• 6 oz. lean meat/protein 6 servings bread/starch
  4 servings fruit 5 or more servings vegetables
  2 servings dairy (low fat preferred) 3 servings
  fat

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Exercise

• Exercise Before diabetic patients engage in
  exercise program, they should consult with their
  healthcare provider because they need to have a
  complete history and physical examination
• Exercise includes anything that keeps them move
• Exercise (total of about 30 minutes a day, at
  least 5 days a week) lowers blood sugar levels by
  improving cell uptake of glucose, causing the
  body to process glucose faster.

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Oral Anti-diabetic Agent

• Biguanides-Metformin (Glucophage) Lowers glucose
  by decreasing liver glucose release and by
  decreasing cellular insulin resistance
• Alpha-Glucose Inhibitors (Precose)-Slows
  digestion and absorption of carbohydrates to
  maintain normal blood glucose levels.
• Meglitinides (Prandin)-Stimulates pancreas to
  secrete insulin
• Thiazolidinediones (Avandia, Actos)-Increases
  insulin sensitivity at receptor sites on liver,
  muscle, and fat cells. The medication works by
  helping make your cells more sensitive to
  insulin. The insulin can then move glucose from
  your blood into your cells for energy.

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Insulin
Type(Trade Name) Onset of Action Peak Duration Nursing Intervention
Rapid-acting (Clear) Insulin Lispro (Humalog) Insulin Aspart (Novorapid) 10-15min 60-90min 4-5hrs Take with meals or may be taken before or after meals
Short Acting/Regular Insulin (Novolin ge Toronto (R) or Humulin R) (clear) 30-60 2-4hrs 5-8hrs Take 30 min before meals
Intermediate-acting (NPH/Lente)(cloudy) 1-4hrs 4-12hrs 18-24hrs
Ultra Lente and Glargine (clear) 4-8hrs 18hrs 24-38hrs Note Glargine can not be mixed with any other insulin
Premixed 10/90, 20/80, 30/70, 40/60, 50/50(cloudy) ideal time to give patients with their premixed? 30 min before their meal, with their meal and after their meal Drawing up Insulin Clear then cloudy to avoid contaminating the clear insulin
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Methods of delivery insulin

• Intravenous (IV)
• Syringes (SC)
• Pens
• Jet injectors
• Insulin pumps

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Site Selection Where can I give the Injections?

• 4 major areas
• Arms-posterior surface
• Abdomen-avoid 1 inch area around navel
• Thighs-anterior surface
• Hips
• Note
• Systematic rotation of injection sites within an
  anatomic area to prevent lipodystrophy.
• Administering each injection 0.5-1inch away from
  the previous injection.

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Storing and Handling Insulin

• Stored at room temperature (15 to 30C).
• If stored in a refrigerator, unopened bottles are
  good until the expiration date printed on the
  bottle.
• Opened bottles that are stored in a refrigerator
  should be used within one month of being opened.
• Protect your insulin (bottles, pens, and
  cartridges) from extremes of hot and cold.
• Never store your insulin in the freezer - once
  insulin is frozen, it loses its potency.

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Diabetes Mellitus

• Case Study

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Patient profile

• Name J.P . Age 68
• Sex Male Ethnicity Algonquin Canadian
• Ht 57 Wt 276 lb (BMI 43.2, obese)
• Medical Hx
• Type II diabetes for 5 years
• hypertension, A-fib
• hypercholesterolemia
• and chronic bronchitis
• Family Hx
• Father died of CVA.
• Mother died of End-stage renal failure due to
  complications of diabetes.
• Social Hx
• Elderly, lives alone
• Sedentary lifestyle
• Poor understanding of diabetes and non-compliance
  of medication

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Risk factors for diabetes

•  Being
• A member of a high-risk group (Aboriginal,
  Hispanic, Asian, South Asian or African descent)
• Overweight, or obese
• Having
• A parent, brother or sister with diabetes
• Health problems e.g. renal, hepatic
• Given birth to a baby that weighed more than 4 kg
  (9 lb)
• Had gestational diabetes (diabetes during
  pregnancy)
• Impaired glucose tolerance or impaired fasting
  glucose
• High blood pressure
• High cholesterol or other fats in the blood

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Assessments on arrival in ER

• V/S T 38.5C HR 145bpm RR 21 BP 80/45
  mmHg (lying) SaO2 88 RA
• CBG 34.0 mmmol/L
• Integumentary poor skin turgor, cracked lips and
  very dry mucosa membrane very dry and flaky
  skin on both feet and up to knees, the skin on
  the lower leg and feet is red and shiny in
  characteristics. One pea-size lesion on the side
  of baby toe of right foot.
• Mental Status Lethargy, confused and
  disoriented, audio and visual hallucination
• poor on people, place and time.
• Neurology unable to feel left side of body,
  sensation of right side of body present.
• c/o dizziness and mild generalized headache.
  Blurry vision.
• Pulmonary respiration shallow. Lungs clear.
  Decreased AE to both lower lobes of lungs.
• Cardiovascular rapid, thready and irregular
  pulse, cool extremities peripheral
• pulses present and weak.
• GI Abd distended and firm. No c/o pain on
  palpation. Decreased and faint bowel sounds .
  Last BM unknown.

Doctor ordered diagnostic tests CT scan of
brain, Cardiac marks, BUN, Creatinine, Chemical
Routines, Electrolytes, CBC, and UA STAT.
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Selected Lab Values
Lab Tests Lab values Normal Values (gt60 years)
CBG HbA1c 34.3 mmol/L 14 3.3-6.1 mmol/L 4-7
CT of brain No structural or anatomic abnormalities are noted
CK 105 units/L 38-174 units/L
Troponin 0.28mcg/ lt0.35 mcg/L
Myoglobin 74 mcg/L lt90 mcg/L
BUN 25 mmol/L (H) 2.9-8.2 mmol/L
Creatinine 170 umol/L (H) 62-115 umol/L
Urinalysis (Dipstick) Urine CS Glucose present Bacteria positive (dipstick) Ketones absent Protein Present Bacteria gt105/ml (positive) Negative Negative Negative Negative Negative
RBC Hgb Hct WBC Serium Osmolality 6.2 X1012/L (H) 18.8 g/dL (H) 55 (H) 15X109/L (H) 350 mOsm/L (H) 4.5-5.9 X1012/L 14-17.5 g/dL 41.1-50.4 4.4-11X109/L 280-300 mOsm/L
Electrolytes Na K CL Ca Mg 125 mEq/L (L) 2.9mEq/L (L) 85 mEq/L (L) 7.8mg/dL (L) 1.5 mg/dL 136-145mEq/L 3.5-5.1 mEq/L 97-107 mEq/L 8.6-10.0mg/dL 1.5-2.3 mg/dL
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• Acute Complications of Diabetes Mellitus

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Acute complications of diabetes

• Hypoglycemia
• Hyperglycemia
• DKA
• Hyperglycemic Hyperosmolar Nonketotic Syndrome
  (HHNS)

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Hypoglycemia

• Hypoglycemia can result from Skipping meals, an
  excess of either insulin or oral diabetes
  medication.
• CBG 2.7-3.3mmol/L
• Usually, hypoglycemia can be managed by consuming
  a sugar product or fruit juice.
• Most hypoglycemic reactions are mild, and people
  with diabetes and their families are trained to
  recognize them and self-administer the sugar
  needed to correct the situation.
• In the case of severe low blood sugar resulting
  in coma the use of glucagon and/or the assistance
  of a health professional may be required.

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Management of Hypoglycemia

• Patient should recognize ss of hypoglycemia
  (sweating, shaking, weakness, hunger, nausea,
  irritability and confusion) and know what to do
  when it strikes
• In case of hypoglycemia, the patient should drink
  a glass of orange juice/regular soft drink, two
  packets of sugar, or 5 or 6 hard candies.
• If the symptoms are still present after 10-15
  minutes, patient should be given again another
  glass of orange juice.
• Once the symptoms have improved, the patient
  should eat longer lasting carbohydrate such as
  bread or milk.

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Management of hypoglycemia

• SC or IM Glucagon or IV dextrose is administered
  (Unconscious Patients/Unable to Swallow)
• Note High-fat foods and high-protein foods
  should not be used initially to correct
  hypoglycemia. These food sources are metabolized
  too slowly to be effective as immediate
  treatment.

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Hyperglycemia

• Patient should recognize symptoms of
  hyperglycemia (high blood sugar) blurred vision,
  excess thirst, frequent urination, and
  nauseaetc.
• Hyperglycemia develops when there is too much
  glucose, not enough insulin or insufficient
  insulin activity in the blood stream.

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Hyperglycemia
Gastrointestinal absorption of glucose
Impaired insulin secretion
Pancreas
HYPERGLYCEMIA
Liver
Muscle
Increased basal hepatic glucose production
Decreased insulin-stimulated glucose uptake
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Management of Hyperglycemia

• Rehydration-if dehydrated, drink plenty of water.
• Oral anti-diabetic agent
• Insulin

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Diabetic ketoacidosis (DKA)

• This is a life threatening disease caused by the
  absence of insulin, which results in disorders in
  the metabolism of carbohydrates, fats, and
  proteins
• Most often occurs in type I diabetes

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Sequence of events

• Serum glucose level rises because most tissues
  cannot utilize glucose without insulin
• The high osmotic pressure created by excess
  glucose leads to osmotic diuresis
• Polyuria occurs
• The sympathetic nervous system responds to the
  cellular need for fuel by converting glycogen to
  glucose and manufacturing additional glucose
• As glycogen stores are depleted, the body begins
  to burn fat and protein for energy
• Fat metabolism produces acidic substances called
  ketone bodies which accumulate and lead to
  metabolic acidosis
• Protein metabolism results in the loss of lean
  muscle mass and a negative nitrogen balance.

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SS for DKA

• The individual with DKA has hyperglycemia,
  ketonuria, and acidosis with a pH of less than
  7.3 or a bicarbonate level of less than 15mmol/L
• Early signs of DKA are anorexia, headache and
  fatigue. As the condition worsens the classic
  signs of polyuria, polydipsia, and polyphagia
  occurs.
• If untreated, the individual becomes dehydrated,
  weak, lethargic with abdominal pain, nausea and
  vomiting, fruity breath, increased respiratory
  rate, tachycardia, blurred vision and
  hypothermia. Late signs are air hunger, coma,
  shock and death

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Assessments

• Blood glucose test (varies from 16.6 to
  44.4mmol/L)
• Blood and urine ketone measurements
• Arterial blood gas analysis

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Treatment

• It is aimed at the correction of the three main
  problems
• Dehydration,
• Electrolyte imbalance,
• Metabolic acidosis.

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Hyperosmolar Hyperglycemia Nonketotic Syndrome
(HHNS)

• Is a condition whereby hyperosmolarity and
  hyperglycemia predominates with alteration in
  sensorium.
• The basic defect is lack of effective insulin.
  The individual persistent hyperglycemia causes
  osmotic diuresis and glucosuria, dehydration,
  hypernatremia and increased osmolarity occurs.
• This condition occurs in the elderly with history
  of, or undiagnosed type 2 diabetes.
• In this situation there is insulin present but
  the level of insulin is enough to prevent fat
  breakdown but not enough to prevent
  hyperglycemia, thus there is no production of
  ketone bodies and no ketoacidosis.

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Manifestations

• Profound dehydration, poor skin tugour,
  tachycardia and alteration in sensorium
• Assessments include
• - Blood glucose levels
• - Electrolytes
• - BUN
• - Complete blood count
• - Serum osmolarity
• - Arterial blood gas analysis
• - Mental status changes

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Comparison of DKA HHNS
Variables DKA Mild DKA Moderate DKA Severe HHNS
Plasma glucose level (mmol/L) gt13.9 gt13.9 gt13.9 gt 33.3
Arterial pH level 7.25 to 7.30 7.00 to 7.24 lt 7.00 gt7.3 (normal)
Serum bicarbonate level(mEq/L) 15-18 10-15 lt10 gt15 (normal)
Urine or serum ketones Positive Positive Positive Small or negative
Effective serum osmolality (mOsm /kg) 300-350 300-350 300-350 gt320
BUN and Creatinine levels Elevated Elevated Elevated Elevated
Alternative sensoria in mental obtundation Alert Alert to drowsy Stupor to coma Stupor to coma
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Comparison of DKA HHNS (cont)

• Characteristics DKA HHNS
• Pts most commonly affected Type I or II, but more
  common in type I Type I or II, but
• more common in type II
• Precipitating event Omission of
  insulin Infection, surgery, CVA,
• Physiologic stress MI
• (infection, surgery, CVA, MI)
• Onset Rapid (lt24h) Slower (over several
  days)
• S S -Acetone breath (a fruity odor) -no
  change in breath ordor
• -Dehydration -Profound dehydration
• -Anorexia, nausea, vomiting, abd
  pain -nausea, vomiting, distended abd
• -Blurred vision -Blurred vision
• -Hypotension -Hypotension
• -Kussmauls respiration -shallow
  respiration
• -Polydipsia, Polyuria, Polyphagia -lethagy,
  mental status
• -Weak, rapid pulse changes

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Mr. J.P. Has

• weakness,
• visual disturbance,
• Nausea and vomiting (but are much less frequent
  than in patients with diabetic ketoacidosis).
• lethargy, confusion, hemiparesis (often
  misdiagnosed as cerebrovascular accident)

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Precipitating Factors in Hyperosmolar
Hyperglycemic State

• Medications
• Calcium channel blockers
• Chemotherapeutic agents
• Chlorpromazine (Thorazine)
• Cimetidine (Tagamet)
• Glucocorticoids
• Loop diuretics
• Thiazide diuretics
• Olanzapine (Zyprexa)
• Phenytoin (dilantin)
• Propranolol (inderal)
• Total parenteral nutrition
• Non-compliance
• Substance abuse
• Alcohol
• Cocaine
• Undiagnosed diabetes

• Coexisting diseases
• Acute MI
• CVA
• Cushing's syndrome
• Hyperthermia
• Hypothermia
• Pancreatitis
• Pulmonary embolus
• Renal failure
• Severe burns
• Infection
• Pneumonia
• Urinary tract infection
• Cellulitis
• Dental infections
• Sepsis

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The Tx of hyperosmolar hyperglycemic state

• Involves five approaches
• Vigorous intravenous rehydration
• Electrolyte replacement
• Administration of insulin
• Diagnosis and management of precipitating and
  coexisting problems

Prevention, prevention and prevention
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In ER

• IV N/S 1000ml _at_ 500 ml/hr continuous infusion.
  Then given Humulin R. 10U IV bolus, followed by
  5U/h continuous infusion in N/S.
• O2 therapy 3L/min via NP.
• Indwelling Catheter in. Monitor IO.
• Pt. on Telemetry to monitor his heart.

Two hours later
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Physicians order

• Meds
• IV solution changed to 1000ml N/S with 40 mEq KCL
  _at_ 250 ml/hr
• continuous infusion. IV solution may change to
  2/3 1/3 with 40mEq KCL
• _at_125ml/hr when CBG lt10 mmol/L.
• Novolin 30/70 SQ 36U Qam, and 20U Qpm ac meals.
• S.S. insulin Humulin R 5U SQ if CBGgt15, 10U if
  CBGgt25
• Metformin 500 mg po bid with meals
• Cipro 400mg q12h infused over 60 minutes.
• Atorvastatin (Lipitor), 10 mg od
• Ramipril 5mg od,
• Digoxin 0.125 mg po od,
• Coumedin 2mg po od,
• Furosemide 80mg po od.
• O2 therapy 3L/min prn
• ventolin i neb q4h prn
• T.E.D stocking (Knee high) on both legs
• V/S q8h if Temp V/S q4h, and CBG (30 min before
  B,L,S, HS)
• Diet Diabetic diet and snacks
• Activity AAT

Mr. J.P. is now transferred to 4 West NBGH
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Dx on admission

• Hyperglycemia or HHNS (CBGgt33.3mmol/L)
• Uncontrolled type 2 diabetes (HbA1c gt7 and by
  medical hx)
• UTI

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Medical Hx

• Obese (BMI 43.2 kg/m2 )
• Hypercholesterolemia
• Peripheral diabetic neuropathy (distal and
  symmetrical by exam)
• Diabetic retinopathy (blurry vision)
• Hypertension (by previous chart data)
• A-fib (by previous chart data and ECG)

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Nursing Dx

• Deficient fluid volume/risk for imbalanced fluid
  volume r/t diabetes complications, polyuria,
  vomiting
• Self-care management/lifestyle deficits r/t
• Limited exercise
• Non-compliance of medication.
• No SMBG program   
• Knowledge deficits r/t poor understanding of
  diabetes

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Nursing Assessments _at_ 0400

• V/S Temp 38.1 C P 150bpm RR 28. BP
  170/100 mmHg SaO2 88
• CBG 10 mmol/L
• Pulmonary Respiration shallow and rapid. Moist
  fine crackles present throughout all lung
  fields. Decreased AE to both lungs. Dyspnea on
  exertion. Cyanosis. Productive coughing with
  frothy sputum.
• Cardiovascular HR 150 bpm pulse bounding and
  irregular. c/o chest pain.
• Abdominal c/o abdominal pain and bloating.
• GI Nauesa
• Integumentary 1 pitting edema on both feet up
  to lower calf. Pallor and skin cool to touch.
• Genitourinary Foley catheter in place draining
  lt60 ml clear yellow urine for the last two hour.
• Mental Status lethargy, confused, disoriented,
  anxious and agitated.

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Nursing Interventions

• J.P. was put on High-Fowlers position with legs
  elevated. O2 via mask _at_ 15L.
• Physician notified. IV continuous infusion D/Ced.
  Saline lock started on the left hand. Nitro-spray
  x3, five minutes apart. Digoxin 0.125mg IV push.
  Furosemide 80mg IV push and Morphine 1mg IV push
  and Gravol 50mg IM administrated as per ordered.

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Education, Education, Education

• Client Teaching (also involve J.P.s daughter)
  re
• SMBG
• Insulin injection,
• Importance of adherence to medication regime
• Appropriate footwear for diabetes, foot care and
  eye care
• Recognition, self-treatment, and prevention of
  hyperglycemia and hypoglycemia
• Know when need to seek for medical attention
• Purchase and wear the diabetes medical bracelet
• Diet meal planning with family members
• Exercise
• Family members need to check on J.P. at least
  once a day

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Referrals

• Referral to CCAC
• Nursing visits 5 times per week for the first two
  weeks. Teaching/Reinforce SMBG and insulin
  injection.
• Home care service (groceries, prepare meals and
  housework)
• Referral to Kipawa Reserve Health Center,
  Diabetes Clinic
• Additional follow-up education on the disease of
  diabetes and the management of diabetes is
  arranged with a diabetes clinic educator in
  Kipawa Reserve
• Join diabetes support group
• Join BP and CBG monitoring program.

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• Chronic Complications
• of Diabetes Mellitus

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Chronic Complications of DM

• Diabetic Neuropathies
• Microvascular Disease
• Retinopathy
• Diabetic nephropathy
• Macrovascular Disease
• CAD
• CVA
• PVD
• Infection
• Lower-limb amputations

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Diabetic Neuropathies

• A group of diseases that affect all types of
  nerves including peripheral (sensorimotor),
  autonomic, and spinal nerves.
• The most common cause of neuropathy
• The most common complication of diabetes
• The prevalence is similar for type I and type II
• Most commonly affects the distal portions of the
  nerves, especially the nerves of the lower
  extremities. AKA Peripheral Neuropathy.

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Diabetic Neuropathies (cont)

• Peripheral neuropathy
• Paresthesias (prickling, tingling, or hightened
  sensation) on feet and fingers.
• Burning sensations (especially at night)
• The feet become numb as the neuropathy progress.
• Decreased sensations of pain and temperature.
  (risk for injury and undetected foot infection)
• A decrease in proprioception (awareness of
  posture and movt of body and of position and wt.
  of objects in relatio to the body)
• A decrease sensation of light touch (may lead to
  unsteady gait)

68
Diabetic Neuropathies (cont)

• Autonomic Neuropathies
• Affecting almost every organ system of the body
• Cardiovascular tachy HR orthostatic
  hypotension and silent, or painless myocardial
  ischemia and MI.
• GI Delayed gastric emptying, bloating, nausea
  and vomiting. Diabetic constipation or
  diarrhea. Unexplained wide swings in blood
  glucose levels r/t inconsistent absorption of the
  glucose form ingested foods secondary to the
  inconsistent gastric emptying.
• Renal Urinary retention, a decreased sensation
  of bladder fullness. Neurogenic bladder. UTI (due
  to neurogenic bladder, inability to completely
  empty the bladder
• (This is especially in pt. with poorly
  controlled diabetes, because hyperglycemia
  impairs resistance to infection)

69
Diabetic Neuropathies (cont)

• Autonomic Neuropathies
• Hypoglycemic unawareness due to diminished or
  absent adrenergic symptoms of hypoglycemia such
  as shakiness, sweating, nervousness, and
  palpations associated with hypoglycemia.
  (autonomic neuropathy of the adrenal medulla)
• Sudomotor neuropathy a decrease or absence of
  sweating of the extremities. Dryness of the feet
  increases the risk for the development of foot
  ulcers.
• Sexual dysfunction impotence in men. Deceased
  libido, vaginal infection, UTI in women.

70
Macrovascular Disease

• Blood vessel walls thicken, atherosclerosis, and
  become occluded by plaque.
• CAD
• The most common cause of death in those with type
  II, also common in those with type I.
• MI (coronary artery occlusion)
• CHF
• CVA-hypertension accelerated atherosclerosis,
  formation of an embolus
• SS of CVA may be similar to symptoms of
  acute diabetic complications e.g. HHNS. It is
  important to rapidly assess the CBG so that
  testing and tx of CVA can be initiated if
  indicated.
• PVD gangrene occurs. Occlusions of the small
  arteries and arterioles lead to the gangrene of
  the lower extremities results in patchy areas of
  the feet and toes. Amputation of foot or leg.

71
Microvascular Disease

• Persistent exposure to hyperglycemia is an
  important factor in the development of diabetic
  microvascular complications.
• Microvascular changes are unique to diabetes.
• Microangiopathy (Diabetic microvascular disease)
  
• Thickening of capillary basement membrane results
  in decreased tissue perfusion. Hypoxia and
  ischemia of various organs may result from
  microangiopathy two areas often affected are the
  retina and the kidney. (persistent increased
  blood glucose levels are responsible for the
  thickening of the basement of membrane)
• Renal retinal syndrome the vast majority of
  individuals with DM have some degree of
  retinopathy, and retinopathy is closely
  associated with diabetic nephropathy.
• Retinopathy
• Diabetic Nephropathy

72
Microvascular Disease
73
Retinopathy

• Diabetic retinopathy is the leading cause of
  blindness in people b/w 20 and 74 years old.
• A change in vision (caused by the rupture of
  small microaneurysms in retinal vessels.)
• Blurred vision (macular edema)
• Sudden loss of vision ( retinal detachment)
• Cataracts ( lens opacity)

74
Diabetic Nephropathy

• Renal disease secondary to diabetic
• microvascular changes in the kidney.
• A common complication of diabetes.
• About 20 to 30 of people with type I or type
  II diabetes develop nephropathy.
• With the blood glucose levels elevated, the
  kidneys filtration mechanism is stressed. The
  earliest sign is a thickening in the glomerulus,
  allowing blood proteins to leak into the urine.
  As a result, the pressure in the blood vessels of
  the kidney increases. The elevated pressure
  stimulates the development of nephropathy.

75
Infections

• The individual with DM is at increased risk for
  infection throughout the body
• Diminished sense
• Microvascular macrovascular complications cause
  decreased O2 supply to tissue. The increased
  content of glycosylated hemoglobin in the red
  blood cell impedes the release of O2 to tissues.
• Pathogens are able to multiply rapidly because
  the increased glucose in body fluids provides an
  excellent source of energy.
• Decreased blood supply resulting from vascular
  changes, leads to decreased supply of WBC to the
  affected area
• The function of the WBC is impaired.

76
Foot and Leg problems

• Typical Diabetic foot ulcer

77
Foot and Leg problems

• 50to 75 of lower extremity amputations are
  performed on people with diabetes.
• Complications of diabetes that contribute to the
  increased risk of foot infections
• Neuropathy Sensory neuropathy leads to loss of
  pain and pressure sensation, and autonomic
  neuropathy leads to increased dryness and
  fissuring of the skin. Motor neuropathy results
  in muscular atrophy.
• PVD Poor circulation of the lower extremities
  contributes to poor wound healing and the
  development of gangrene.
• Immunocompromise Hyperglycemia impairs the
  ability of specialized leukocytes to destroy
  bacteria. Thus, in poorly controlled diabetes,
  there is lowered resistance to infections.

78
Management of hospitalized diabetic patients

• 10 to 20 of general med-surg patients in the
  hospital have diabetes. This number may increase
  as elderly patients make up a greater proportion
  of the population.
• Often diabetes is not the primary reason for
  hospitalization, yet problems with the control of
  diabetes frequently result from changes n the
  pts normal routine or from surgery or illness.

79
Management of hospitalized diabetic patients

• Avoid hyperglycemia during hospitalization
• Assess the pts usual home routine. Try to
  approximate as much as possible the home schedule
  of insulin, meals, and activities.
• CBG monitoring. The insulin doses must not be
  withheld when CBG are normal.
• IV antibiotics should be mixed in NS to avoid
  excess infusion of dextrose.
• Tx of hypoglycemia/hyperglycemia by following
  hospital protocol.

80
Management of hospitalized diabetic patients
(cont)

• Avoid hypoglycemia during hospitalization
• Hypoglycemia in a hospitalized pt. is usually the
  result of too much insulin or delays in eating.
• To avoid hypoglycemic reactions caused by delayed
  food intake, the nurse should arrange for a snack
  if meals are going to be delayed because of
  procedures, PT, or other activities.

81
Management of hospitalized diabetic patients
(cont)

• NPO
• For the pt who must have NPO in preparation for
  diagnostic or surgical procedure, the nurse must
  ensure that the usual insulin dosage has been
  changed.
• Even when no food is taken, glucose levels may
  rise as a result of hepatic glucose production,
  especially in pts with type I diabetes.
  Elimination of the insulin dose may lead to the
  development of DKA.
• Administering insulin to the patient with
  type I diabetes who is NPO is an important
  nursing intervention.
• Because DKA does not develop when insulin doses
  are eliminated in type II diabetes pts, skipping
  the insulin dose may be safe, but close
  monitoring is essential.
• Glucose testing and insulin administration should
  be at regular intervals usually 2-4 times per
  day.
• Pts should receive dextrose infusion to provide
  some calories and limit ketosis.
• To prevent these problems resulting from the need
  to withhold food, diagnostic tests and procedures
  and surgery should be scheduled early in the
  morning if possible.

82
Management of hospitalized diabetic patients
(cont)

• Hygiene
• Must focus attention on oral hygiene and skin
  care, because diabetic pts are at increased risk
  for periodontal disease.
• Keep the skin clean and dry, especially in areas
  of contact b/w two skin surfaces (eg, groin,
  axilla, and in obese women, under the breasts).
• For the bedridden diabetic pt, nursing care must
  emphasize the prevention of skin breakdown at
  pressure points. The heels are particularly
  susceptible to breakdown.
• Feet should be cleaned, dried, lubricated with
  lotion (but not b/w the toes), and inspected
  frequently.
• Teach the pt about diabetes self-management,
  including daily oral, skin, and foot care.
• Female diabetic pts should also be instructed
  about measures for the avoidance of vaginal
  infections, which occur more frequently when
  blood glucose levels are elevated.

83
Management of hospitalized diabetic patients
(cont)

• Diabetes and the risk of blood clots
• Higher risk of DVT formation than non-diabetic
  pts.
• The factors that increase the risk of DVT.
• Age gt60 years
• Recent major surgery
• Poor circulation Lack of adequate circulation in
  the deep veins can lead to a blood clot.
• Obesity Being significantly overweight affects
  your circulation and your activity levels.
• Infections
• Interventions
• Anticoagulant e.g. Heparin
• T.E.Ds
• Encourage ambulation/leg exercise

84
References

• Beers, M., Porter, R., Jones, T., Kaplan, J.,
  Berkwits, M. (2006). The Merck Manual of
  Diagnosis and therapy. Eighteenth Edition. Merck
  Research laboratories.
• Canadian Diabetes Association (nd). Diabetes
  Facts. Retrieved on Oct 2, 2007 from
• http//www.diabetes.ca/Section_About/thefacts.as
  p
• Canadian Diabetes Association (n.d). Foot care A
  step toward good health. Retrieved on Oct 12,
  2007 from http//www.diabetes.ca/Section_About/fe
  et.asp
• Demir, I., Ermis, C.,  Altunbas, H.,  Balci, M.
  K.(2001). Serum HbA1c Levels and Exercise
  Capacity in Diabetic Patients. Jpn Heart J. 42
  (5), 607-616. Retrieved on Oct. 12, 2007 from
  http//sciencelinks.jp/j-east/article/200207/00002
  0020702A0062021.php
• Malarkey, L., McMorrow M. (2005). Saunders
  Nursing Guide to Laboratory and Diagnostic
  Tests. Elsevier Saunders
• Mayhall, R. (n.d.) Diabetes and the risk of blood
  clots. Retrieved on Oct. 20, 2007 from
  http//www.helium.com/tm/201996/thrombosis-blood-
  clots-known
• McCance, K, Huether, S.E. (2002).
  Pathophysiology the biologic basis for disease in
  adults children. Mosby.

85
References

• Public Health Agency of Canada (n.d). Diabetes.
  Retrieved on Oct. 13, 2007 from
  http//www.phac-aspc.gc.ca/ccdpc-cpcmc/diabetes-d
  iabete/english/index.html
• Smeltzer, S. C. Bare, B.G.(2004). Brunner
  Suddarths textbook of Medical-Surgical Nursing.
• Lippincott Williams Wilkins.
• Stoner, G. D. (2005) Hyperosmolar Hyperglycemic
  State. American Family Physician 71(9).
  1723-1730. Retrieved on Oct 2/07 from
  http//www.aafp.org/afp/20050501/1723.pdf
• News Release(November 14, 2002). Health Canada
  launches diabetes public awareness campaign
  Retrieved on Oct 2/07 from http//www.hc-sc.gc.ca/
  ahc-asc/media/nr- cp/2002/2002_75_e.html