Diabetes Mellitus
Physiology
of Energy Metabolism

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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.
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.
Pathophysiology
of Diabetes Mellitus

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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
Pathophysiology
of 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.
Classical manifestations of
diabetes

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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
Types of diabetes

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Type I
Type II
Gestational diabetes
Type I

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
.
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
S&S
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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

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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.
S&S

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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
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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
S&S
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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 S&S 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 (con’t)
Diagnostic criteria for DM and impaired glucose
regulation
Test
CBG
FPG
Normal
Impaired
glucose
regulation
3.3-6.1mmol/L
<5.6mmol/L
5.6-6.9mmol/L
OGTT <7.7mmol/L
HbA1c 3%-6%
Diabetes
>7.0mmol/L
7.7-11.0mmol/L >11.1mmol/L
>7%
HbA1c
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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.
Management of
Diabetes
Good Diabetes Management
Regular Blood Glucose Monitoring
Regular Exercise
Healthy Nutrition
Nutrition
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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.
Nutrition (con’t)
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 (<30% 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

Exercise

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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.
Oral Anti-diabetic Agent

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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.
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
Premixed: 10/90, 20/80,
30/70, 40/60, 50/50
(cloudy)
Note: Glargine can not be mixed with any other insulin
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

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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:

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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
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Stored at room temperature (15 to 30°C).
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.
Diabetes Mellitus
Case Study
Patient profile
Name: J.P
.
Age: 68
Sex: Male
Ethnicity: Algonquin Canadian
Ht: 5’7” 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 pregnancy)
 Impaired glucose tolerance or impaired fasting glucose
 High blood pressure
 High cholesterol or other fats in the blood
Assessments on arrival in ER
V/S: T: 38.5°C ; 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 (>60 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/
<0.35 mcg/L
Myoglobin
74 mcg/L
<90 mcg/L
BUN
25 mmol/L
Creatinine
170 umol/L (H)
62-115 umol/L
Urinalysis
(Dipstick)
Glucose: present
Bacteria: positive (dipstick)
Ketones: absent
Protein: Present
Negative
Negative
Negative
Negative
Urine C&S
Bacteria: >10^5/ml (positive)
Negative
RBC
Hgb
Hct
WBC
Serium Osmolality
6.2 X10^12/L (H)
18.8 g/dL
(H)
55%
(H)
15X10^9/L
(H)
350 mOsm/L (H)
4.5-5.9 X10^12/L
14-17.5 g/dL
41.1%-50.4%
4.4-11X10^9/L
280-300 mOsm/L
Electrolytes:
Na+
K+
CLˉ
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
(H)
2.9-8.2 mmol/L
Acute Complications
of Diabetes Mellitus
Acute complications of diabetes
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Hypoglycemia
Hyperglycemia
DKA
Hyperglycemic Hyperosmolar Nonketotic
Syndrome (HHNS)
Hypoglycemia
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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.
Management of Hypoglycemia

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Patient should recognize s&s 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 treatment.
Hyperglycemia


Patient should recognize symptoms of
hyperglycemia (high blood sugar): blurred
vision, excess thirst, frequent urination,
and nausea…etc.
Hyperglycemia develops when there is too
much glucose, not enough insulin or
insufficient insulin activity in the blood
stream.
Hyperglycemia
Gastrointestinal absorption of glucose
Impaired insulin secretion
Pancreas
HYPERGLYCEMIA
Liver
Increased basal hepatic
glucose production
Muscle
Decreased insulin-stimulated
glucose uptake
Management of Hyperglycemia

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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 proteins
Most often occurs in type I diabetes
Sequence of events
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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.
S&S 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
Assessments



Blood glucose test (varies from 16.6 to
44.4mmol/L)
Blood and urine ketone measurements
Arterial blood gas analysis
Treatment

It is aimed at the correction of the three main
problems:

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
Dehydration,
Electrolyte imbalance,
Metabolic acidosis.
Hyperosmolar Hyperglycemia
Nonketotic Syndrome (HHNS)

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
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.
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

Comparison of DKA & HHNS
Variables
DKA
Arterial pH level
Serum bicarbonate
level
(mEq/L)
DKA
HHNS
Mild
Plasma glucose level
(mmol/L)
DKA
>13.9
7.25 to 7.30
Moderate
Severe
>13.9
>13.9
7.00 to 7.24
< 7.00
> 33.3
>7.3 (normal)
15-18
10-15
<10
Urine or serum
ketones
Positive
Positive
Positive
Effective serum
osmolality (mOsm
/kg)
300-350
300-350
300-350
>320
Elevated
Elevated
Elevated
Elevated
Alert to drowsy
Stupor to coma
BUN and
Creatinine levels
Alternative
sensoria in mental
obtundation
Alert
>15 (normal)
Small or negative
Stupor to coma
Comparison of DKA & HHNS
(con’t)
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
Physiologic stress
(infection, surgery, CVA, MI)
Infection, surgery, CVA,
MI
Onset
Rapid (<24h)
Slower (over several days)
S&S
-Acetone breath (a fruity odor)
-Dehydration
-Anorexia, nausea, vomiting, & abd pain
-no change in breath ordor
-Profound dehydration
-nausea, vomiting, distended
abd
-Blurred vision
-Hypotension
-shallow respiration
-lethagy, mental status
changes
-Tachycardia
-Neurological deficits,
-seizures
-Blurred vision
-Hypotension
-Kussmaul’s respiration
-Polydipsia, Polyuria, & Polyphagia
-Weak, rapid pulse
-Weakness
Treatment
-Insulin
-Rehydration
-Correct metabolic acidosis
& electrolyte imbalance
- Insulin (play a less critical
role in tx of HHNS.
-Rehydration
-correct electrolyte imbalance
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
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
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
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…
In ER




IV: N/S 1000ml @ 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 I&O.
Pt. on Telemetry to monitor his heart.
Two hours later…
Physician’s order:
Meds:

IV solution changed to 1000ml N/S with 40 mEq KCL @ 250 ml/hr
continuous infusion. IV solution may change to 2/3 &1/3 with 40mEq KCL
@125ml/hr when CBG <10 mmol/L.

Novolin 30/70 SQ 36U Qam, and 20U Qpm ac meals.

S.S. insulin: Humulin R 5U SQ if CBG>15, 10U if CBG>25

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
Diagnostic Tests: Repeat Electrolyte, CBC, BUN, Creatinine, ECG, PT, INR, and Urinalysis.
Mr. J.P. is now transferred to 4 West NBGH…
Dx on admission



Hyperglycemia or HHNS (CBG>33.3mmol/L)
Uncontrolled type 2 diabetes (HbA1c >7%
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, 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
Nursing Assessments @ 0400:







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
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 <60 ml clear yellow urine for
the last two hour.
Mental Status: lethargy, confused, disoriented, anxious and agitated.
Nursing Interventions
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J.P. was put on High-Fowler’s position with
legs elevated. O2 via mask @ 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) 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
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.
Chronic Complications
of Diabetes Mellitus
Chronic Complications
of DM
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Diabetic Neuropathies
Microvascular Disease
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Macrovascular Disease
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Retinopathy
Diabetic nephropathy
CAD
CVA
PVD
Infection
Lower-limb amputations
Diabetic Neuropathies
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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 (con’t)

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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 mov’t 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 (con’t)
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 (con’t)



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.
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
** S&S 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.
Microvascular Disease
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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
Retinopathy
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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
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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 kidney’s
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.
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.
Foot and Leg problems

Typical Diabetic foot ulcer
Foot and Leg problems
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50%to 75% of lower extremity amputations are
performed on people with diabetes.
Complications of diabetes that contribute to the
increased risk of foot infections:
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
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
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
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 pt’s normal routine or from surgery or
illness.
Management of hospitalized
diabetic patients
Avoid hyperglycemia during hospitalization

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Assess the pt’s 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 (con’t)
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 (con’t)
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.
Management of hospitalized
diabetic patients (con’t)
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.
Management of hospitalized
diabetic patients (con’t)

Diabetes and the risk of blood clots
 Higher risk of DVT formation than non-diabetic pts.
 The factors that increase the risk of DVT.
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Age: >60 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
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.asp

Canadian Diabetes Association (n.d). Foot care: A step toward good health. Retrieved on Oct 12,
2007 from http://www.diabetes.ca/Section_About/feet.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/200207/000020020702A0062021.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.
References

Public Health Agency of Canada (n.d). Diabetes. Retrieved on Oct. 13, 2007 from
http://www.phac-aspc.gc.ca/ccdpc-cpcmc/diabetes-diabete/english/index.html

Smeltzer, S. C. & Bare, B.G.(2004). Brunner & Suddarth’s 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