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Diabetes Mellitus


Diabetes Mellitus Physiology of Energy Metabolism All body cells use glucose for energy. To maintain this constant source of energy, blood glucose levels must be kept ... – PowerPoint PPT presentation

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Title: Diabetes Mellitus

Diabetes Mellitus
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
  • 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.

  • 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.

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
  • 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

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
  • 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.

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

Types of diabetes
  • Type I
  • Type II
  • Gestational diabetes

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
  • Glucose derived from food is not stored in the
    liver but remains in the blood stream and
    contributes to postprandial (after meals)
  • .

  • 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

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
  • These patients are not prone to the development
    of DKA.

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

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.

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
  • Having high blood pressure

  • 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

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.

Diagnosis of diabetes (cont)
  • Diagnostic criteria for DM and impaired glucose

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
  • 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
  • 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.

  • Management of Diabetes

Good Diabetes Management
  • Regular Blood Glucose Monitoring
  • Healthy Nutrition 

Regular Exercise
  • 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
  • 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.

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
  • 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

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  • 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.

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
Methods of delivery insulin
  • Intravenous (IV)
  • Syringes (SC)
  • Pens
  • Jet injectors
  • Insulin pumps

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.

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
  • 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.

Diabetes Mellitus
  • Case Study

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

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
  • Impaired glucose tolerance or impaired fasting
  • High blood pressure
  • High cholesterol or other fats in the blood

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.
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
  • Acute Complications of Diabetes Mellitus

Acute complications of diabetes
  • Hypoglycemia
  • Hyperglycemia
  • DKA
  • Hyperglycemic Hyperosmolar Nonketotic Syndrome

  • Hypoglycemia can result from Skipping meals, an
    excess of either insulin or oral diabetes
  • 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.

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.

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

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

Gastrointestinal absorption of glucose
Impaired insulin secretion
Increased basal hepatic glucose production
Decreased insulin-stimulated glucose uptake
Management of Hyperglycemia
  • Rehydration-if dehydrated, drink plenty of water.
  • Oral anti-diabetic agent
  • Insulin

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
  • Most often occurs in type I diabetes

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.

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
  • 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

  • Blood glucose test (varies from 16.6 to
  • Blood and urine ketone measurements
  • Arterial blood gas analysis

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

Hyperosmolar Hyperglycemia Nonketotic Syndrome
  • Is a condition whereby hyperosmolarity and
    hyperglycemia predominates with alteration in
  • 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.

  • 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

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
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
  • 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
  • -Polydipsia, Polyuria, Polyphagia -lethagy,
    mental status
  • -Weak, rapid pulse changes

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)

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

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

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)

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

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.

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.

Education, Education, Education
  • Client Teaching (also involve J.P.s daughter)
  • 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

  • Referral to CCAC
  • Nursing visits 5 times per week for the first two
    weeks. Teaching/Reinforce SMBG and insulin
  • Home care service (groceries, prepare meals and
  • 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.

  • Chronic Complications
  • of Diabetes Mellitus

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

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.

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)

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)

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
  • Sexual dysfunction impotence in men. Deceased
    libido, vaginal infection, UTI in women.

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
  • 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.

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

Microvascular Disease
  • 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)

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.

  • 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.

Foot and Leg problems
  • Typical Diabetic foot ulcer

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.

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.

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.

Management of hospitalized diabetic patients
  • 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.

Management of hospitalized diabetic patients
  • 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
  • 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
  • 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.

Management of hospitalized diabetic patients
  • 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
  • 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.

Management of hospitalized diabetic patients
  • Diabetes and the risk of blood clots
  • Higher risk of DVT formation than non-diabetic
  • 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

  • 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
  • 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
  • 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
  • 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
  • McCance, K, Huether, S.E. (2002).
    Pathophysiology the biologic basis for disease in
    adults children. Mosby.

  • Public Health Agency of Canada (n.d). Diabetes.
    Retrieved on Oct. 13, 2007 from
  • 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
  • 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
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