DIABETES MELLITUS

Definition - It is a chronic, progressive, metabolic disorder characterized by elevated

blood glucose level in blood due to defect in insulin secretion, insulin action or both.

It is a disease caused by an imbalance between insulin intake supply and insulin demand
and characterized by high blood glucose level.

Diabetes mellitus is a chronic, progressive, metabolic disorder disease, characterized by

the body’s inability to metabolize carbohydrates, fats and protein, leading to
hyperglycemia (High blood glucose level).

Insulin is secreted by the beta cells of the islets of Langerhans and works to lower the
blood glucose level after meals by facilitating the uptake and utilization of glucose by
muscle, fat, and liver cells.

Types –

1. Type –I Diabetes mellitus (IDDM) (5% - 10%) – Insulin Dependent Diabetes

Mellitus is caused by destruction of pancreatic beta cells. Causes of destruction is
through a combination of genetic, immunological and environmental factors.
Helps to beta cell destruction. Certain Histo Compatibility Agents (HCA) also help
in destruction of beta cell of pancreas. Previously known as juvenile diabetes
mellitus, ketosis prone diabetes, brittle diabetes. Onset is usually young  30
years of age.

2. Type – II Diabetes mellitus (NIDDM) (90% - 95%) - Non Insulin Dependent

Diabetes Mellitus occurs due to insulin resistance and impaired insulin secretion.
Insulin resistance refers to decreased sensitivity of tissues to insulin or insulin
becomes less effective to stimulating glucose uptake by tissue. It is caused by
strong hereditary component often associated with symptoms of fatigue, weight
gain, poor wound healing and recurrent infection. It found primarily in adults
over 30 years of age. Previously known as adult onset diabetes, maturity onset
diabetes, ketosis resistant diabetes, stable diabetes.
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 3. Gestational diabetes mellitus (GDM) – increased blood glucose level during
pregnancy is called Gestational Diabetes mellitus. It is because of secretion of
placental hormone, which inhibit the action of insulin. GDM is associated with
increased risk of fetal mobility. Onset during pregnancy, usually in the second or
third trimester. Occurs in 2% - 5% of all pregnancy.

4. Diabetes mellitus associated with other conditions or syndromes (ADA) –

previously classified as secondary diabetes mellitus. It is accompanied by
conditions known or suspected to cause the disease such as pancreatic diseases,
hormonal abnormalities, medications such as corticosteroids and estrogen
containing preparations.

5. Prediabetes – prediabetes is classified as Impaired Glucose Tolerance (IGT) and

Impaired Fasting Glucose (IFG). They are refers to a condition in which blood
glucose concentrations fall between normal levels and those considered
diagmostic for diabetes. IFT is 2 hours post glucose level 140 – 199 mg/dl. IFG is
fasting blood glucose i.e. 100 – 125 mg/dl.

Etiology and risk factors –

 Family history of D.M

 Obesity
 Advance age  45years
 Hypertension
 History of gestational diabetes during pregnancy
 Race / Ethicity – Africans, Americans
 Failure of production of insulin
 Hereditary
 Impaired glucose tolerance
 Chronic use of drugs like corticosteroids, thiazide diuretics
 Increased level of fat

Pathophysiology –

Type – II Diabetes mellitus (NIDDM)

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 Due to etiological factors

(insulin resistance and impaired insulin secretion)

Increase production of insulin and decrease sensitivity of tissues to insulin

Glucose level is maintained or slightly elevated

Type – II Diabetes mellitus

Type – I Diabetes mellitus (IDDM)

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 Due to etiological factors

Destruction of pancreatic beta cells

Inability to produce insulin

Insulin deficiency

Impaired fat metabolism Imbalance of glucose level

↓ ↓

Impair fat metabolism Increase concentration of glucose in blood

↓ ↓

Breakdown of fat in cells Kidneys may not reabsorb all of the

filtered glucose (osmotic dieresis)
↓
↓

Weight loss
Glucose in urine
↓
↓

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 Increase appetite (Polyphagia) due to
decrease storage of calories
Increased loss of fluid by urination
(Polyuria)

Increased thirst (Polydipsia)

Clinical manifestation –

 3 P’s = polyurea, polydipsia and polyphagia

 Fatigue and weakness
 Sudden vision changes (blurred vision)
 Tingling or numbness in hands or feet
 Dry skin, sore that are slow to heal
 Recurrent infection
 Nocturia
 Nausea and vomiting
 Abdominal pain
 Lethargy
 Pruritis
 Weight loss
 Skin infection
 Vaginitis
 Ketonuria
 Dizziness
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Diagnostic evaluation –

1. Blood glucose test –

a. Fasting blood sugar (FBS)  140 mg/dl
Normal  115 mg/dl

b. Post prandial glucose – (PP1 – 2 hours after lunch and PP2 – 2 hours after
dinner)
Diabetes mellitus  200mg/dl

Normal  140 mg/dl

c. Random blood glucose –

Diabetes mellitus ≥ 200 mg/dl

Normal  140 mg/dl

2. Glucose tolerance test (GTT) - oral glucose tolerance test (OGTT) is a fasting
glucose is  140 mg/dl and OGTT result of the 2 hours plasma glucose
measurement between 140 mg/dl and 200 mg/dl with one interventing value
greater than 200 mg/dl after a 75 gm glucose intake.

3. Urine test – urine test for presence of glucose in urine (glycosuria), albumin
(albuminurea) and ketone body (ketoneurea)

Management – the main goal of diabetes treatment is to normalize insulin activity and
blood glucose levels to reduce the development of vascular and neuropathic
complications.

1. DIETARY MANAGEMENT – main objectives to dietary management are control of

total caloric intake to attain or maintain a reasonable body weight, control of
blood glucose level and normalization of lipids and blood pressure to prevent
heart disease. Nutritional management of diabetes has following goals –
a. To achieve and maintain
 Blood glucose levels in the normal range or as close to normal.
 A lipid and lipoprotein profile that reduces the risk for vascular disease.
 Blood pressure level in the normal range or as close to normal.
b. To prevent or slow, the rate of development of the chronic complications by
modifying nutrients intake and lifestyle.

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 c. To address individual nutrition needs, taking into account personal and
cultural preferences and willingness to change.
d. To maintain the pleasure of eating by only limiting food choices when
indicated by scientific evidence.

o Meal planning and related teaching –

 Meal planning should concern the patient’s food preferences, lifestyle,
usual eating times and ethnic and cultural background.
 The first step in preparing a meal plan is a thorough review of the patient’s
diet history to identify his or her eating habits and life style. This includes
thorough assessment of the patient’s need for weight loss, gain, or
maintenance. In most instances, people with type-2 diabetes require
weight reduction.

o Caloric requirements – caloric controlled diets are planned by first calculating a

person’s energy needs and caloric requirements based on age, gender, height,
and weight. An activity level is then factored in to provide the actual number of
calories required for weight maintenance. To promote a 1 to 2 pound weight loss
per week, 500 to 1000 calories are subtracted from the daily total. The calories
are distributed into carbohydrates, proteins, and fats and a meal plan is then
developed, taking into account the patient’s lifestyle and food preferences.

o Caloric distribution – a meal plan for diabetes focus on the percentages of

calories that come from carbohydrates, proteins and fats.
CHO – CHO foods have greatest effect on blood glucose level because they are
more quickly digested than other foods and are converted into glucose rapidly.
Carbohydrate consist of sugar (sucrose) and starch (rice, pasta, bread). Low
glycemic index diets may reduce postprandial glucose level. Therefore, the
nutrition guidelines recommended that all carbohydrate should be eaten in
moderate to avoid high postprandial blood glucose leve.

Fat – reducing the total percentage of calories from fat sources and limiting the
amount of saturated fats. Limiting the total intake of dietary cholesterol.

Protein – meal plan may include the use of some nonanimal sources of protein
(legumes, whole grains).

Fiber – increase fibre in diet may improve blood glucose level, decrease the need
for insulin and lower total cholesterol and low density lipoprotein level in the
blood.

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o Food classification system – to teach dietary principles and to help in meal
planning, several systems have been developed in which foods are organized into
groups with common characteristics, such as number of calories, composion of
food, or effect on blood glucose level. Several of these are listed here –

Exchange list – a commonly used tool for nutritional management is the

exchange lists for meal planning. There are 6 main exchange lists – bread /starch,
vegetable, milk, meat, fruit and fat. Meal plans can be based on a recommended
number of choices from each exchange list.

Nutrition labels – food manufacturer are required to have the nutrition content
of foods listed on package labels. The label should includes information about
how many grams of carbohydrate are in a serving of food. Carbohydrate counting
is a nutritional tool used for blood glucose management because CHO are the
main nutrients in food that influence the blood glucose levels. This method
provides flexibility in food choices, can be less complicated to understand than
the diabetis food exchange list.

Healthy food choice – it is an alternative to counting grams of carbohydrate is

measuring serving or choices. It is similar to food exchange list and emphasizes
portion control of total servings of carbohydrate at meals and snacks.

Food guide Pyramid – it is another tool used to develop meal plans. Foods that
are lowest in calories and fat and highest in fiber should make up the basis of the
diet.

Glycemic index – the term glycemic index is used to describe how much a given
food increases the blood glucose level compared with an equivalent amount of
glucose.

2. EXERCISE – exercises lowers blood glucose level by increasing the uptake of

glucose by body muscles and by improving insulin utilization. It also improves
circulation and muscle tone. Exercise also alter blood lipid concentrations,

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 increasing levels of high density lipoproteins and decreasing total cholesterol and
triglyceride levels. Regular daily exercise should be encouraged. Avoid heavy
exercises. Use proper footwear. Avoid exercise in extreme heat or cold. Inspect
feet daily after exercise. Avoid exercise during periods of poor metabolic control.

3. MONITORING GLUCOSE LEVELS AND KETONES –

o Self Monitoring of Blood Glucose (SMBG) –

 SMBG allows for detection and prevention of hypoglycemia and
hyperglycemia.
 Various methods for SMBG are available. Most involve obtaining a dro of
blood from the fingertip, applying the blood to a special reagent strip and
allowing the blood to stay on the strip for the amount of time specified by
the manufacturer (usually 5 to 30 seconds). The meter gives a digital
readout of the blood glucose value.
 Some meters are binosensors that can use blood obtained from alternative
test sites, such as the forearm. They have a special lancing device that is
useful for patients who have painful fingertips or experience pain with
fingersticks.
 Laboratory methods measure plasma glucose, most blood glucose
monitors approved for patient’s use in the home and some test strips
calibrate blood glucose reading to plasma value.
 Plasma glucose values are 10% to 15% higher than whole blood values, and
it is crucial for patients with diabetes to know whether their monitor and
strips provide whole blood or plasma results.
 Factors affecting SMBG performance include visual acuity, fine motor
coordination, cognitive ability, comfort with technology and willingness to
use it and its cost.
 The important hazard of all methods of SMBG is that the patient may
obtain and report erroneous blood glucose values as result of using
incorrect techniques. Some common sources of error include improper
application of blood (drop too small), damage to the reagent strips caused
by heat or humidity, use of outdated strips, and improper meter cleaning
and maintenance.
 Nurse play should teach to patient SMBG technique and evaluating the
techniques of patients. The accuracy of the meter and strip should be
assessed, specially whenever a new vial of strips is used and whenever the
validity of the reading is in doubt.

o Candidates for self monitoring of blood glucose – SMBG is a useful tool for
managing self care for patient with diabetes. For patient with type -2 diabetes,
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 SMBG is recommended during periods of suspected hyperglycemia or
hypoglycemia and when the medication or dosages of medication is modified. It
is recommended for patients with –
 Unstable diabetes (severe swings from very high to very low blood glucose
levels with in a 24 hours of day)
 A tendency to develop severe ketosis or hypoglycemia
 Hypoglycemia without warning symptoms.

o Frequency of self monitoring of blood glucose –

 For patient who take insulin, SMBG is recommended 2-4 times daily
(usually before meals and at bed time).
 For patients who take insulin before each meal, SMBG is required at least 3
times daily before meals to determine each dose.
 Patient who do not receiving insulin may be instructed to assess their
blood glucose levels at least 2 or 3 times per week, including a 2-hour
postprandial test.
 For all patients, testing is recommended whenever hypoglycemia or
hyperglycemia is suspected, with changes in medications, activity, or diet
and with stress or illness.

o Responding to self monitoring of blood glucose results – patient are asked to

keep a record or logbook of blood glucose level so that they can detect patterns.

o Using a Continuous Glucose Monitoring System (CGMS) - a CGMS can be used

to continuously monitor blood glucose levels. A sensor attached to an infusion
set, which is similar to an infusion pump infusion set, is inserted subcutaneously
in the abdomen and connected to the device worn on a belt. After 72 hours, the
data from the device are downloaded, and blood glucose reading are analyzed. It
can be used to determine whether treatment is adequate over a 24 hours period.

o Testing for glycated hemoglobin – glycated hemoglobin (also referred to as

glycosylated hemoglobin, HgbA1c or AIC) is a blood test that reflects average blood
glucose levels over a period of approximately 2-3 months. When blood glucose
levels are elevated, glucose molecules attach to hemoglobin in red blood cells.
The longer the amount of glucose in the blood remains above normal, the more
glucose binds to hemoglobin and the higher the glycated hemoglobin level
becomes. This complex (hemoglobin attach to the glucose) is permanent and
lasts for the life of the individual red blood cell, approximately 120 days. If the
blood glucose values are consistently high, then the test result is also elevated. If
the patient reports mostly normal SMBG results but the glycated hemoglobin is

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 high, there may be error in the methods used for glucose monitoring, errors in
recording results or frequent elevations in glucose levels at times during the day
when the patient is not usually monitoring blood sugar levels.

o Testing for Ketones (Ketone bodies) – ketones or ketone bodies are byproducts
of fat breakdown, and they accumulate in the blood and urine. Ketones in the
urine signal that there is a deficiency of insulin and control of type – 1 diabetes in
deteriorating. The risk of DKA is high. When there is almost no effective insulin
available, the body starts to break down stored fat for energy. Urine testing is the
most common method used for self-testing of ketone bodies by patients. Most
commonly, the patient uses a urine dipstick (ketostix or Chemstrip uK) to detect
ketonuria. The reagent pad on the strip turns purple when ketones are present.
(one of the ketone bodies is called acetone, and this term is frequently used
interchangeably with the term ketones). Other strips are available for measuring
both urine glucose and ketones (Keto-Diastix or Chemstrip uGK). Large amount of
ketones may depress the color response of the glucose test area.
Urine ketone testing should be performed whenever patient with type -1
diabetes have glycosuria or persistently elevated blood glucose levels (more than
240 mg/dl for two testing periods in a row) and during illness, in pregnancy with
preexisting diabetes, and in gestational diabetes.

4. PHARMACOLOGICAL MANAGEMENT –
a. Insulin therapy – in type – 1 diabetes exogenous insulin must be administered
for life because the body loses the ability to produce insulin. In type -2
diabetes, insulin is necessary on a long term basis to control glucose level if
diet and oral agents are ineffective. When administering insulin, it is very
important to read the label carefully and to be sure that the correct type of
insulin is administered. it is also important to avoid mistaking Lantus insulin
for Lente insulin and vice versa.

o Preparations – a number of insulin preparations are available. They vary

according to 3 main characteristics : time course of action, species (source), and
manufacturer.
Time course of action – insulin is grouped into several categories based on the
onset, peak, and duration of action. Human insulin preparations have a shorter
duration of action than insulin from animal sources because the presence of
animal proteins triggers an immune response that results in the binding of animal
insulin, which slow its availability.

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  Rapid acting insulin produce rapid onset of action, therefore patient is
instructed to eat with in 5 to 15 minutes soon after administration of rapid
acting insulin.
 Short acting insulin are called regular insulin (marked R on the bottle).
Regular insulin is a clear solution and is usually administered 20-30 minutes
before meal. Regular insulin is the only insulin approved for I.V use.
 Intermediate acting insulins are called NPH insulin (Neutral Protamine
Hagedorn) or Lente insulin. They are similar in their course of action,
appear white and cloudly.
 Very long acting insulin is are called peakless or basal insulin. It absorb
slowely and given once a day.

Time Course Agent Onset Peak Duration Indication

of action

Rapid-acting Lispro (humalog) 10-15 1 hr. 2-4 hr. Used for rapid
min reduction of
glucose level, to
treat
postprandial
hyperglycemia,
Aspart (novolog) 5-15 min 40-50 min 2-4 hr.
and to prevent
G nocturnal
hypoglycemia
Lulisine (apidra) 5-15 min 30-60 min 2 hr.

Short-acting Regular ½ - 1 hr. 2-3 hr 4-6 hr Usually

(humalog R, administered
novolin R, iletin II 20-30 min
Regular) before a meal,
may be taken
alone or in
combination
with longer
acting insulin.

Intermediate- NPH (neural 2-4 hr. 4-12 hr. 16-20 hr. Usually taken
acting protamine after food
hagedorn)

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 Novolin L (Lente) 3-4 hr. 4-12 hr. 16-20 hr.

Novolin N (NPH)

Very long- Glargine (lantus) 1 hr. Continuous 24 hrs. Used for basal
acting (no peak) dose.
Detemir
(levemir)

Species (sources) – insulin is obtained from human and animal. Animal sources
are beef (cow), pork (pig) pancreas. Human insulin preparations have a shorter
duration of action than insulin from animal sources because the presence of
animal proteins triggers an immune response that results in the binding of animal
insulin, which slow its availability.

o Complication of insulin therapy –

 Local allergic reactions – a local allergic reaction includes redness, swelling,
tenderness and induration or a 2-4 cm wheal. They may appear at the
injection site 1-2 hours after the insulin administration. These reactions,
which usually occur during the beginning stages of the therapy and
disappear with continued use of insulin, are becoming rare because of the
increased use of human insulins. The physician prescribe an antihistamine
to be taken I hour before the injection, if such a local reaction occurs.

 Systemic allergic reactions – systemic allergic reactions to insulin are rare.

There is an immediate local skin reaction that gradually spreads into
generalized urticaria (hives). Occasionally associated with generalized
edema or anaphylaxis. The treatment is desensitization, with small dose of
insulin administred in gradually increasing amounts using a desensitization
kit.

 Insulin Lipodystrophy – it refers to a localized reaction, in the form of

either lipoatrophy or lipohypertrophy, occurring at the site of insulin
injections. Lipoatrophy is loss of subcutaneous fat, it appears as slight
dimpling or more serious pitting of subcutaneous fat (development of
fibrofatty masses at the injection site). It is caused by the repeated use of
an injection site. If the insulin is injected into scarred areas, absorption may
be delayed. This is the reason that rotation of injection sites is important.

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 Patient should avoid injecting insulin into these areas until the hypertrophy
disappears.

 Resistance to injected insulin – clinical insulin resistance has been defined

as a daily insulin requirement of 200 units or more. Most patients have
some degree of insulin resistance at one time or another. This may occur
for various reasons, the most common being obesity. In most of the
patients with diabetes who take insulin, immune antibodies develop and
bind the insulin, thereby decreasing the insulin available for use. Treatment
consists of administering a more concentrated insulin preparation, such as
U500, which is available by special order. Ocationally prednisolone is given
to block the production of antibodies. This may be followed by a gradual
reduction in the insulin requirement. Therefore, patients must monitor
their blood for hypoglycemia.
 Morning hyperglycemia – an elevated blood glucose level on arising in the
morning is caused by an insufficient level of insulin, which may be caused
by several factors –
Insulin waning – progressive rise in blood glucose from bedtime to
morning. Treatment include – increase evening (predinner or bed time)
dose of intermediate-acting or long-acting insulin, or institute a dose of
insulin before the evening meal if one is not already part of the treatment
regimen.

Dawn phenomenon – relatively normal blood glucose until about 3 AM,

when the level begins to rise. Treatment include – changing time of
injection of evening intermediate-acting insulin from dinner time to bed
time.

Somogyi effect – normal oe elevated blood glucose at bedtime, a decrease

at 2-3 AM to hypoglycemic levels, and a subsequent increase caused by the
production of counter regulatory hormones. Treatment include – decrease
evening (predinner or bed time) dose of intermediate-acting insulin, or
increase bedtime snack.

o Methods of insulin delivery –

 Insulin pens – insulin pens use small (150-300 unit) prefilled insulin
cartridges that are loaded into a pen like holder. A disposable needle is
attached to the device for insulin injection. Insulin is delivered by dialing in
a dose or pushing a button for every 1or 2 unit increment administered.
these devices are most useful for patients who need to inject only one type

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 of insulin at a time (eg. Pre meal rapid-acting insulin 3 times a day and
bedtime NPH insulin) or when can use the premixed insulins. These pens
are convenient for those who administer insulin before dinner if eating out
or traveling. They are also useful for patients with impaired manual
dexterity, vision, or cognitive function, which makes the use of traditional
syringes difficult.

 Jet injectors – they are an alternative to needle injections. They deliver

insulin through the skin under pressure in an extremely fine stream. These
devices are more expensive and require thorough training and supervision
when first used. Patient should be cautioned that absorption rates, peak
insulin activity, and insulin levels may be different when changing to a jet
injector.(insulin administered by jet injector is usually absorbed faster).

 Insulin pumps – continuous subcutaneous insulin infusion involves the use

of small, externally worn devices (insulin pumps) that closely mimic the
functioning of the normal pancreas. Insulin pumps contain a 3 ml syringe
attached to a long (24-42 inch), thin, narrow-lumen tube with a needle or
Teflon catheter attached to the end. The patient inserts the needle or
catheter into subcutaneous tissue (usually on the abdomen) and secures it
with tape or a transparent dressing. The needle or catheter is changed at
least every 3 days. The pump is then worn either on a belt or in a pocket.
Some women keep the pump tucked into the front or side of the bra or
wear it on a garter belt on the thigh. Insulin is delivered by subcutaneous
infusion at a basal rate (eg. 0.5 to 2 units/hr). when a meal is consumed,
the patient calculates a dose of insulin by counting the total amount of
CHO for the meal using a predetermined insulin-to-carbohydrate ratio. For
eg. A ratio of 1 unit of insulin for every 15 gm of carbohydrate would
require 3 units for a meal with 54 gm of CHO. This allows flexibility of meal
timing and content. The most common risk of insulin pump therapy is
ketoacidosis, which can occur if there is an occlusion in the infusion set or
tubing. The patient should be taught to administer insulin by manual
injection if an insulin interruption is suspected.

Disadvantages –

 Disruption in the flow of insulin from the pump that may occur if the
tubing or needle becomes occluded, if the supply of insulin runs out,
or if the battery is depleted. Effective teaching is required to
minimize this risk.
 Infection at needle site
 Hypoglycemia
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  Inconvenient to wear the pump for 24 hours.

 Future insulin delivery – researches into mechanical delivery of insulin has

involved implantable insulin pumps that can be externally programmed
according to the blood glucose test results. Clinical trials with these devices
are continuing. In addition, there is research into the development of
implantable devices that both measure the blood glucose level and deliver
insulin as needed. Methods of administering insulin by the oral route (oral
spray or capsule) and skin patch are undergoing intensive study.

 Transplantation of pancreatic cells – transplantation of the whole pancreas

or a segment of the pancreas is being performed on a limited people
(mostly patients with diabetes who are receiving a kidney transplantation
simultaneously). Implantation of insulin producing pancreatic islet cells is
another approach under investigation.

b. Oral antidiabetic or hypoglycemic agents – oral antidiabetic agents are

effective for patients who have type -2 diabetes that can not be treated
effectively with MNT and exercise alone. They are no longer be effective in
controlling diabetes because of decline in function of beta cells. Eg.
 First generation sulfonylureas – acetohexamide (dymelor),
chlorpropamide (diabines), tolazamide (tolinase), tolbutamide (orinase)
 Second generation sulfonylureas – glipizide (glucotrol), glyburide
(micronase), glimepiride (amaryl)
 Biguanides – metformin (glucophage)
 Alpha-Glucosidase inhibitors – acarbose (precise), miglitol (glyset)
 Non sulfonylurea insulin secretagogues – repaglinide (prandin),
nateglinide (starlix)
 Thiazolidinediones (Glitazones) – pioglitazone (actos), rosiglitazone
(avandia)
 Dipeptidyl peptidase-4 (DPP-4) inhibitors – sitagliptin (januvia),
vildagliptin (galvus)

c. Other therapy – pramlintide (symlin), exenatide (byetta) are two new drugs
used in management of diabetes. Both are injectable drugs.
Pramlintide (symlin) – is a hormone that is secreted by the beta cells of the
pancreas, used in treatment of both type-1 and type-2 diabetes. It is used to
control hyperglycemia in adults who have not achieved acceptable levels of
glucose control despite the use of insulin at mealtimes. It is used with insulin,
not in place of insulin.
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 Exenatide (byetta) – it is used for treatment of type-2 diabetes in combination
with metformin or sulfonylureas. It is derived from a hormone that is
produced in the small intestine. It is normally released after food is ingested to
delay gastric emptying and inhance insulin secretion. Exenatide must be
injected twice a day within 1 hour before breakfast and dinner. It is not a
substitute for insulin.

5. Surgical management –
a. Pancreas transplantation - transplantation of the whole pancreas or a
segment of the pancreas is being performed on a limited people (mostly
patients with diabetes who are receiving a kidney transplantation
simultaneously).
b. Islet cells (pancreatic cell) transplantation - Implantation of insulin producing
pancreatic islet cells is under investigation as a treatment for type-1 diabetes.
Less toxic anti-rejection drugs are required for this procedure.

Nursing management –

1. Risk for fluid volume deficit related to polyurea and dehydration.

2. Altered nutrition less than body requirement related to imbalance of insulin
activity, physical activity.
3. Knowledge deficit related to diabetes self care.
4. Anxiety related to fear of inability to manage diabetes and it’s complications.

Health education –

1. Diet –
 Providing all essential food constituents such as vitamin, minerals
 Meeting energy needs of patient
 Low carbohydrate and low fat diet
 Weight reduction for type-2 diabetes mellitus
 Avoid rich carbohydrate foods such as jiggery, honey, sugarcane juice,
sweet potato.
 Teach meal planning
 Daily weight checking

2. Life style changes –

 Prevent any injury or trauma
 Low carbohydrate and low fat diet

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  Weight reduction for type-2 diabetes mellitus
 Avoid rich carbohydrate foods such as jiggery, honey, sugarcane juice,
sweet potato.
 Wear foot wears while walking, to prevent foot injury .
 Daily exercise
 Avoid heavy exercises

3. Foot care –
 Assess skin of feet and legs for sensation, injury, dryness
 Use monofilament sensation test of feet
 Protect feet from injury by –
 Using heel protectors, foot cardle for patient with bed rest
 Avoiding applying drying agents to skin
 Apply skin moisturizer.
 Inspect foot carefully daily for corns, blisters, abrations, redness and nail
abnormality.
 Massage feet with absorbable agents
 Prevent moisture between the toes.
 Wear well fitting, comprehensive shoes and socks. Shoe and soacks should
be long enough, wide enough, soft and low healed.
 Avoid rubber or plastic soles shoe which cause the feet to excessive
sweating and aggrevate fungal infection.
 Advice to always wear shoe or sleepers while walking.
 Avoid walking with beared feet.

4. Teaching self monitoring blood glues (SMBG) –

 Teach various methods of checking blood sugar.
 Teach correct technique for SMBG
 Advice to maintain logbook or keeping record of BSL values.

5. Teaching self administration of insulin – insulin injection is self administered into

the subcutaneous tissue with the use of special insulin syringes. The information
includes -
 Storing insulin –
 Insulin vials not in use, should be refrigerated. Extremes of
temperature should be avoided, insulin should not be allowed to
freeze and should not be kept in direct sunlight.
 The insulin vial in use should be kept at room temperature to reduce
local irritation at the injection site, which may occur if cold insulin is
injected.

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  The patient should be instructed to always have a spare vial of the
type or types of insulin he or she uses.
 Cloudy insulin should be thoroughly mixed by gently inverting the
vial or rolling it between the hands before drawing the solution into
a stringes or a pen.
 Bottles of intermediating-acting insulin should also be inspected for
flocculation, which is a frosted, whitish coating inside the bottle.
This occurs most commonly with human insulins that are exposed to
extremes of temperatire. It should not be used.

 Selecting syringes –
 Syringes must be matched with the insulin concentration (eg. U-
100). U-100, i.e. there is 100 units per ml or cc.Currently, three sizes
of U-100 insulin syringes are available :
1 ml syringes that hold 100 units.

0.5 ml syringes that hold 50 units

0.3 ml syringes that hold 30 units.

 Mixing insulins – the important issues are –

 That pataients be consistent in technique, so as not to draw up the
wrong dose in error or the wrong type of insulin
 That patients not inject one type of insulin into the bottle containing
a different type of insulin. Injecting cloudy insulin into a vial of clear
insulin contaminates the entire vial of clear insulin and change its
action.
 For patient who have difficulty in mixing, they may use premixed
insulin,or they may have prefilled syringes prepared, or they may
take 2 injections. Premixed insulins are available in several different
ratios of NPH insulin to regular insulin. The ratio of 70/30 (70% NPH
and 30% regular insulin in one bottle) is most common. This
combination is available as Novolin 70/30 (Novo-Nordisk) and
Humulin 70/30 (Lilly).
 The prefilled syringes should be stored with the needle in an upright
position to avoid clogging of needle.

 Withdrawing insulin – most of the printed material available on insulin

dose preparation instruct patients to inject air into the bottle of insulin
equivalent to the number of units of insulin to be withdrawn. The rationale

xix
 for this is to prevent the formation of a vaccum inside the bottle, which
would make it difficult to withdraw the proper amount of insulin.

 Selecting and rotating the injection sites –

 The four main areas for injection are the abdomen, upper arms
(posterior surface), thighs (anterior surface), and hips. The speed of
absorption is greatest in the abdomen and decreases progressively
in the arm, thigh and hip, respectively.
 Systematic rotation of injection sites within an anatomic area is
recommended to prevent lipodystrophy.
 Patient should not to use the same site more than once in 2 to 3
weeks.
 If the patient is planning to exercise, insulin should not be injected
into the limb that will be exercised, because this will cause the drug
to be absorbed faster, which may result in hypoglycemia.

 Preparing the skin – use of alcohol swab to cleanse the skin is not
recommended. Patient who are using, they should be cautioned to allow
the skin to dry after cleansing with alcohol swab to prevent localized
redness and burning sensation.

 Inserting the needle (Self injection of insulin) –

 With one hand, stabilize the skin by spreading it or pinching up a
large area.
 Pick up syringe with the other hand and hold it as you would a
pencil. Insert needle straight into skin. Some patients may be taught
to insert the needle at a 45° angle.
 To inject the insulin, push the plunger all the way in.
 Pull needle straight out of skin. Press cotton ball over injection site
for several seconds.
 Use disposable syringe only once and disard into hard plastic
container (with a tight-fitting top) such as an empty bleach or
detergent container. Follow state regulations for disposal of syringes
and needles.

 Disposing of syringes and needles

6. Prevention of injury to hypoglycemia –

 Monitor BSL frequently
 Keep ready food before insulin administration.
xx
  Teach sign and symptoms of hypoglycemia like sweating, tremor,
headache, irritability, confusion, lack of co-ordination, increase pulse,
palpitation, nervousness.
 Teach how to treat hypoglycemia. Oral intake of sugar or glucose in water.
 Advice to take some snacks before exercise to prevent hypoglycemia.

Difference between type – I and type – II Diabetes mellitus –

S. Features Type - I Type - II

No.

1. Synonyms Insulin dependent diabetes Non insulin dependenr

mellitus, juvenile diabetes, diabetes mellitus, adult or
laible or brittle diabetes maturity onset diabetes, mild
diabetes

2. Age at onset Usually occurs before age 30 Usually occurs after age 30 yrs,
yrs, but may occur at any age but can occurs in children

3. Incidence About 10% About 90%

4. Types of onset Usually abrupt, with rapid Incidious, may be

onset of hyperglycemia asymptomatic or mildly
asymptomatic, body adapts to
slow onset of hyperglycemia

5. Endogenous Little or none Below normal, normal or

insulin above normal
production

6. Body weight at Ideal body weight or thin 85% of clients are obese, may
onset be ideal body weight

xxi
7. Ketosis Prone to ketosis, usually Resistant to ketosis, can occur
present at onset, often with infection or stress
present during poor control

8. Manifestations Polyuria, polydipsia, Often none, may be mild

polyphagia, fatigue manifestations of
hyperglycemia

9. Dietary Essential Essential

management

10. Exercise Essential Essential

management

11. Exogenous Dependent on insulin for 20% - 30% of clients may

insulin survival require insulin
administration

12. Oral Not effective Effective

hypoglycemic
agents

13. Teaching needs At diagnosis and ongoing At diagnosis and ongoing

Complications –

 Acute complications –
 Hypoglycemia (Insulin reactions)
 Diabetic Ketoacidosis (DKA)
 Hyperglycemic Hyperosmolar Nonketotic Syndrome (HHNKS)

 Chronic complications –
 Macrovascular complications (coronary heart disease, cerebrovascular
disease, hypertension, peripheral vascular disease, infection)
xxii
  Microvascular complications
 Diabetic retinopathy
 Nephropathy
 Diabetic neuropathy
 Foot and leg problems

HYPOGLYCEMIA (INSULIN REACTION)

Hypoglycemia occurs when the blood glucose falls to less than 50 to 60 mg/dl. It occurs
because of too much insulin or oral hypoglycemic agents, too little food, or excessive
physical activity. It can occur at any time of the day or night.

In elderly patients with diabetes, hypoglycemia is a particular concern for many

reasons –

 Elderly people frequently live alone and may not recognize the symptoms of
hypoglycemia.
 With decreasing renal function, it takes longer for oral hypoglycemic agents to be
excreted by the kidneys.
 Skipping meals may occur because of decreased appetite of financial limitations
 Decreased visual acuity may lead to errors in insulin administration.

Etiology and risk factors –

 An overdose of insulin
 Omitting a meal or eating less food than usual
 Overexertion without additional carbohydrate compensation
 Nutritional and fluid imbalance caused by nausea and vomiting
 Alcohol intake

Clinical manifestation –

 Mild hypoglycemia – sweating, tremor, tachycardia, palpitation, nervousness and

excessive hunger, diaphoresis, paresthesis, pallor, shakiness.
 Moderate hypoglycemia – inability to concentrate, headache, lightheadedness,
confusion, memory lapses, numbness of the lips and tongue, slurred speech,

xxiii
 impaired coordination, emotional changes, irrational or combative behavior,
double vision, drowsiness.
 Severe hypoglycemia – disoriented behavior, disorientation, seizures, difficuly
arousing from sleep, loss of consciousness.

Management –

1. Administration of carbohydrates – 15 gm of a fast acting concentrated source of

carbohydrate such as the following, given orally :
 3-4 commercially prepared glucose tablets
 4-6 oz of fruit juice or regular soda
 6-10 hard candies
 2-3 teaspoons of sugar or honey
The BSL is retested in 15 minutes and retreated if it is less than 70-75 mg/dl.

o Mild hypoglycemia – 10-15 gm of CHO, contained in the following –

 4 oz orange juice
 6 oz regular soda
 6-8 oz 2% milk
 6-8 lifesavers candies
 1 small (2 oz) tube of cake icing
 4 tsp granulated sugar
o Moderate hypoglycemia – 20-30 gm of CHO. Glucagon 1 mg S/C or IM

o Severe hypoglycemia – 50% dextrose, 25 gm IV. Glucagon 1 mg S/C or IM

2. Initial emergency management – in emergency, for adults who are unconscious

and cannot swallow, an injection of glucagon 1 mg is administered either
subcutaneously or intramuscularly. Glucagon is a hormone produced by the alpha
cells of the pancreas that stimulates the liver to breakdown glycogen, the stored
glucose. Glucagon is available in the form of powder in a vial and must be mixed
with a diluents immediately before being injected. A concentrate source of
carbohydrate followed by a snack should be given to patient on awakening to
prevent recurrence of hyperglycemia.
In hospitals and emergency departments, for patients who are unconscious or
can not swallow, 25 to 50 ml of 50% dextrose in water (D50W) is administered by
I.V.

xxiv
Other hypoglycemic disorders –

 Hypoglycemic unawareness – it refers to a syndrome in which people with

diabetes are unaware that they are hypoglycemic. Beta adrenergic agents
(propanolol) can cause hypoglycemic unawareness and blunt adrenergic
(epinephrine) effects in clients with diabetes.

 Hyglycemia with rebound hyper glycemia (Somogyi effect) - Hyglycemia with

rebound hyper glycemia, known as the Somogyi effect or somogyi phenomenon.
This phenomenon was implicated in the past as a common cause of fasting
morning hyperglycemia. It usuallt results from excessive evening insulin dosing.
Nocturnal rebound hyperglycemia should be investigated by SMBG levels
between 2AM and 4 PM and again 7 AM. Decreasing the intermediate-acting
insulin dose at supper time, moving the intermediate-acting insulin dose to
bedtime, or increasing the size of the bedtime snack prevent this phenomenon.

 Dawn phenomenon – it refers to an early morning (4 to 8 AM) increase in blood

glucose level without preceding nocturnal hypoglycemia. Dissipation of insulin
dose not appear to be the sole cause of this phenomenon. SMBG and education
about bedtime snacks, manifestations of nocturnal hypoglycemia, and
importance of avoiding hypoglycemia are essential.

DIABETIC KETOACIDOSIS (DKA)

Definition – DKA is an acute complication of diabetes mellitus, characterized by

hyperglycemia, ketonurea, acidosis and dehydration. DKA is caused by an absence or
markedly inadequate amount of insulin. This deficit in available insulin results in
disorders in the metabolism of carbohydrate, protein and fat. It is usually common
complication of type-1 diabetes.

Etiology and risk factors –

 Taking too little insulin

 Skipping doses of insulin

xxv
  Inability to meet an increased need for insulin created by surgery, trauma,
pregnancy, stress, puberty or infection
 Developing insulin resistance through the presence of insulin antibodies

Pathophysiology –

Lack of insulin

Decreased utilization of glucose by muscle, Increased breakdown of fat

fat and liver
↓
Increased production of glucose by liver
Increased fatty acids
↓
↓
Hyperglycemia

↓ ↓

Blurred vision Polyuria Increased ketone bodies

Dehydration ↓ ↓

Acetone Acidosis
breath
↓ ↓
Poor appetite
↓ ↓
nausea
Weakness Nausea Increasingly
rapid
Headach Increased Vomiting
respiration
thirst Abdominal
pain
(Polydipsia)

xxvi
Clinical manifestation –

 Abdominal pain
 Anorexia
 Dehydration
 Fruity odor of ketones on breath
 Hyperpnea or kussmaul’s respirations
 Hypotension
 Impaired level of consciousness or coma
 Nausea and vomiting
 Polyuria
 Polydipsia
 Weakness
 Headache
 Dehydration
 Electrolyte imbalance
 Somnolence
 Tachycardia
 Visual disturbances
 Warm, dry skin
 Weight loss
 Muscle cramps
 Hypotension
 Stupor and coma

Diagnostic evaluation –

 Serum glucose level is usually elevated over 300 mg/dl, may be as high as 1000
mg/dl.
 Serum and urine ketone bodies are present
 Serum bicarbonate and PH are decreased due to metabolic acidosis and PaCO2 is
decreased.
 Serum sodium and potassium level may be low, normal or high due to fluid shifts
and dehydration.
 BUN, creatinine, hemoglobin, and hematocrit are elevated due to dehydration.
 Urine glucose is present in high concentration and specific gravity is increased,
reflecting osmotic dieresis and dehydration.

Management – in addition to treating hyperglycemia, management of DKA is aimed at

correcting dehydration, electrolyte loss, and acidosis.

xxvii
1. Rehydration – rehydration is important for maintaining tissue perfusion. The
patient may need as much as 6-10 litre of IV fluid to replace fluid losses caused by
polyuria, hyperventilation, diarrhea and vomiting.
I.V fluid replacement in diabetic ketoacidosis as :

 Hour-1 – provide 15-20 ml/kg of isotonic sodium chloride (0.9%) normal

saline or full strength Ringer’s lactate (RL).
 Hour-2 – continue fluid as above at 15 ml/kg. if the client is hypernatremic,
has heart failure or is a child, consider half strength sodium chloride (0.45%
normal saline).
 Hour-3 – reduce fluid intake to 7.5 ml/kg in adults. Fluid should be 0.45%
normal saline.
 Hour-4 – adjust fluid intake to meet clinical need. Consider urine output
rate in calculation.
Plasma expanders are necessary to correct severe hypotension that does not

respond to I.V fluid treatment.

2. Restoring electrolytes – the major concerning electrolyte during treatment of

DKA is potassium. The serum level of potassium decreases as potassium reenters
the cells during the course of treatment of DKA, therefore, the serum potassium
level must be monitored frequently. 12-lead ECG is used as a guid for plasma
potassium (K+) concentration. Flattening or inversion of the T wave with U wave
and prolongation of the QT interval indicate hypokalemia. Peaking of T waves,
loss of P wave, and a disturbed QRS complex indicate hyperkalemia. I.V
replacement of potassium is based on plasma K+ concentration. If K+
concentration is :
  3 mEq/L, infuse ≥ 0.6 mEq/kg/hour
 3-4 mEq/L, infuse 0.6 mEq/kg/hour
 4-5 mEq/L, infuse 0.2-0.4 mEq/kg/hour
 6 mEq/L, withhold until K+ concentration is  0.6 mEq/L
Add K+ to replacement fluid therapy. If concentration is 20-40 mEq/L and infusion

into peripheral vein causes irritation, infuse into central vein.

3. Reversing acidosis (correct acidosis) – ketone bodies (acids) accumulate as a

result of fat break-down. The acidosis that occurs in DKA is reversed with insulin,
inhibit fat breakdown, thereby stopping acid buildup. Insulin is usually infused
intravenously at a slow, continuous rate (eg. 5 unit/hr). hourly blood sugar values
must be measured. Regular insulin, the only type of insulin approved for I.V use,
is added to I.V solutions. The nurse must convert hourly rates of insulin infusion
xxviii
 to IV drip rates. For eg. , if 100 units of regular insulin are mixed into 500 ml of
0.9% NS, then 1 unit of insulin equals 5 ml, therefore, an initial insulin infusion
rate of 5 units/hr would equal 25 ml/hr.
When mixing the insulin drip, it is important to flush the insulin solution through
the entire IV infusion set and to discard the first 50 ml of fluid. Insulin molecules
adhere to the inner surface of IV infusion sets, therefore, the initial fluid may
contain a decreased concentration of insulin.

4. Prevent recurrence – to prevent DKA, clients with diabetes should learn to do the
following :
 Take insulin in appropriate doses at appropriate times.
 Monitor BSL frequently, at least before each meal and at bedtime.
 Monitor urine ketone levels when blood glucose level increase to greater
than 250 mg/dl
 Schedule regular appointments with a health care provider to review blood
glucose levels, weight gains or losses, and general state of health and well
being. The first clinical manifestations of infection (upper respiratory tract,
urinary tract, or vaginal infection) should be reported immediately.
 Emphasize that the greatest weapons against DKA are regular, daily SMBG,
adherence to the diabetes management programme, and early recognition
of and intervention in mild ketosis.

Hyperglycemic Hyperosmolar Nonketotic Syndrome (HHNS)

It is a serious condition in which hyperosmolarity and hyperglycemia predominant, with

alterations of the sensorium (sense of awareness). At the sama time, ketosis is usually
minimal or absent. The basic biochemical defect is lack of effective insulin (i.e, insulin
resistance). Persistent hyperglycemia causes osmotic dieresis, which results in losses of
water and electrolytes. To maintain osmotic equilibrium, water shifts from the
intracellular fluid space to the extracellular fluid space. With glycosuria and
dehydration, hypernatremia and increased osmolarity occur.

It is an acute complication of type-2 diabetes characterized by extreme hyperglycemia

(600 to 2000 mg/dl), profound dehydration, mild or undetectable ketonuria, and the
absence of acidosis. It occurs most often in older people (50-70 years of age) who have
no known history of type-2 diabetes mellitus.

xxix
Etiology and risk factors –

 Therapeutic agents –
 Glucocorticoids
 Diuretics
 Dipheylhydration
 Beta-adrenergic blocking agents
 Immunosuppressive agents
 Chlorpromazine
 Diazoxide
 Therapeutic procedures –
 Peritoneal dialysis
 Hemodialysis
 Surgical stress
 Chronic illness –
 Renal disease
 Heart disease
 Hypertension
 Previous stroke
 Alcoholism
 Psychiatric diagnosis
 Loss of thirst
 Acute illness –
 Infection
 Gangrene
 UTI
 Septicemia
 Burns
 G.I bleeding
 MI
 Pancreatitis
 Stroke

Clinical manifestation –

 Hypotension
 Severe hyperglycemia (600-2000 mg/dl)
 No or slight ketosis
 Severe dehydration (dry mucus membranes, poor skin turgor)

xxx
  Hyperosmolality (increased concentration) of plasma and elevated blood urea
nitrogen level
 Tachycardia
 Variable neurologic signs (alteration of sensorium, seizures, hemiparesis).

Diagnostic evaluation –

 Serum glucose and osmolality are greatly elevated

 Seru and urine ketone bodies are minimal to absent
 Serum sodium and potassium levels may be elevated, depending on degree of
dehydration, despite total body losses.
 BUN and creatinine may be elevated due to dehydration.
 Urine and specific gravity is elevated due to dehydration.

Management – sama as DKA.

1. Correct fluid and electrolyte imbalance with I.V fluid.

2. Provide insulin via drip to lower plasma glucose.
3. Evaluate complications, such as stupor, seizures, or shock, and treat
appropriately.
4. Identify and treat underlying illness or events that precipitated HHNS.

Nursing management –

Fluid volume deficit related to severe dehydration

Risk for aspiration related to reduced LOC and vomiting.

Comparison of DKA and HHNS –

S.No. Characteristics DKA HHNS

1. Patient most commonly Can occur in type-1 and Can occur in type-1 and
affected type-2 diabetes, more type-2 diabetes, more
common in type-1 common in type-2
diabetes diabetes, specially
elderly patients with
type-2 diabetes

xxxi
2. Precipitating events Omission of insulin, Physiologic stress
physiologic stress (infection, surgery, CVA,
(infection, surgery, CVA, MI)
MI)

3. Onset Rapid (less than 24 hrs) Slow (over several days)

4. Blood glucose level Usually  250 mg/dl Usually  600 mg/dl

5. Arterial PH  7.3 Normal

6. Serum and urine ketones Present Absent

7. Serum osmolality 300-350 mOsm/L  350 mOsm/L

8. Plasma bicarbonate level  15 mEq/L Normal

9. BUN and creatinine Elevated Elevated

levels

10. Mortality rate  5% 10-40%

DIABETIC RETINOPATHY

Diabetic retinopathy is the leading cause of blindness among people between 20-70
years of age. It occurs in both type-1 and type-2 diabetes.

Definition – it is a retinal disorder characterized by damage to the retinal vessels

(retinal artery or vein), resulting in occlusion of the vessels.

As a result of occlusion of the retinal blood vessels, there is inadequate blood supply to
the retina, cause vision loss.

The retina is richy supplied with blood vessels of all kinds : small arteries and veins,
arterioles, venules, and capillaries. Retinopathy has 3 main stages –

a. Nonprofilerative (background)
b. Preproliferative

xxxii
 c. Proliferative

Clinical manifestation –

 Patient may report “spiders,” “cobwebs” or tiny speaks floating in their vision
 Dark streaks or a red film that blocks vision
 Vision loss, usually in both eyes
 Blurred vision
 A dark or empty spot in the centre of the vision
 Poor night vision
 Difficulty in adjusting from bright light to dim light

Management –

1. Photocoagulation – the goal of the photocoagulation is to stop the leakage of

blood and fluid in the retina and thus slow the progress of diabetic retinopathy.
In this a high energy laser beam creats small burns in areas of the retina with
abnormal blood vessels to seal any leaks. A medical contact lens is placed on the
cornea to help focus laser light on the sections of the retina to be treated.
Fluorescein angiographic photographs may serve as maps to sjow where the laser
burns should be placed. For proliferative diabetic retinopathy, panretinal or
scatter photocoagulation can be used to treat the entire retina except the
macula.

2. Vitrectomy - it is the removal of the blood-filled vitreous. A vitreous cutter cuts

the tissue and removes it, piece by piece, from the eye. The volume of removal
tissue is replaced with saline to maintain the normal shape and pressure of the
eye. During vitrectomy, the surgeon also use a lser probe to perform a procedure
called panretinal photocoagulation to prevent renewed growth of abdominal
blood vessels and bleeding.

NEPHROPATHY

Nephropathy or Renal disease secondary to diabetic microvascular changes in the

kidney, is a common complication of diabetes. Diabetic neuropathy is the single most
common cause of stage-5 chronic kidney disease. It was formally known as end stage of
renal diasease (ESRD). About 35% - 45% of clients with type-1 diabetes are found to
xxxiii
have nephropathy 15-20 years after diagnosis. About 20% of clients with type-2
diabetes are found to have nephropathy 5-10 years after diagnosis. A consequence of
microangiopathy, nephropathy involves damage to and obliteration of the capillaries
that supplies the glomeruli of the kidney. This damage leads manifestations such as
intercapillary glomerulosclerosis, nephrosis, albuminuria and hypertension.

Management –

 Control of hypertension (use of ACE inhibitors such as captopril)

 Prevention or treatment of urinary tract infection
 Avoidance of nephrotoxic substances (eg. Antibiotics, other selected drugs)
 Adjustment of medications as renal function changes
 Low sodium diet
 Low potassium diet

DIABETIC NEUROPATHIES

Neuropathy is the most common chronic complication of diabetes. Near about 60% of
diabetic patient experience it. Diabetic neuropathy refers to a group of disease that
affect all types of nerves, including peripheral (sensoromotor), autonomic, and spinal
nerves. The etiology of neuropathy may involve elevated blood glucose levels over a
period of years. Because nerve fibers do not have their own blood supply, they depend
on the diffusion of nutrients and oxygen across the membrane. When axon and
dendrites are not nourish, their transmission of impulses slows. The causes of diabetic
neuropathy include – vascular insufficiency, chronic elevations in blood glucose level,
hypertension and cigarette smoking.

The 3 most common types of diabetic neuropathy, they are – sensorimotor

polyneuropathy , autonomic neuropathy, and cranial mononeuropathy. Sensorimotor
polyneuropathy is called peripheral neuropathy. Cranial mononeuropathy affecting the
oculomotor nerve, specially occur in the elderly.

 Peripheral neuropathy – peripheral neuropathy most commonly affects the distal

portions of the nerves, specially the nerves of the lower extremities. It affects
both sides of the body symmetrically and spread in a proximal direction.
Initial symptoms may include – paresthesia (prickling, tingling, or heightened
sensation) and burning sensation (specially at night). As the neuropathy
progresses, the feet become numb, a decrease in proprioception (awareness of
xxxiv
 posture and movement of the body and of position and weight of objects in
relation to the body) and a decreased sensation of light touch may lead to an
unsteady gait. Decreased sensation of pain and temperature cause increase risk
for injury and undetected foot infections. Patient may have deformities of foot
and joints (charcot joint).

Management includes – intensive insulin therapy and control of blood sugar level
delay the onset and slow the progression of neuropathy. Pain management
include – analgesic, tricyclic antidepressants, antiseizures (phenytoin sodium,
carbamazepine), antiarrhymic (mexitil), transcutaneous electrical nerve
stimulation (TENS).

 Autonomic neuropathy – neuropathy of autonomic nervous system results in a

broad range of dysfunctions affecting almost every organ system of the body. It
manifests itself in its effect on papillary, cardiovascular, gastrointestinal, and
genitourinary functions.
 Papillary – inability to see in dark, inadequate pupil dilation
 Cardiovascular – orthostatic hypertension, tachycardia
 Gastrointestinal – dysphagia, abdominal pain, nausea, vomiting,
malabsorption, postprandial hypoglycemia, diarrhea, constipation, fecal
incontinence, delayed stomach emptying, feeling of stomach fullness,
anorexia, weight loss,
 Genitourinary – neurogenic bladder, urination, infrequent urge to urinate
with long periods of time between voiding, and a decreased urine stream,
Urinary stasis, UTI. In male erectile dysfunction and retrograde ejaculation.
In female painful intercourse.
Treatment –

 orthostatic hypotension is treated by diet high in sodium, discontinuation

of medications that impeded autonomic nervous system responses, use of
sympathomimetics and other agents (caffeine) that stimulate an
autonomic response, mineralocorticoid therapy, and use of lower body
elastic garments that maximize venous return and prevent pooling of
blood in the extremities.
 Treatment of delayed gastric emptying includes a low fat diet, frequent
small meals, frequent blood glucose monitoring and use of agents that
increase gastric motility (eg. Metoclopramide, bethanechol). Treatment of
diabetic diarrhea include bulk forming laxatives or antidiarrheal agents.
Constipation is treated with a high fiber diet and adequate hydration,
medications, laxatives and enema.

xxxv
 FOOT AND LEG PROBLEMS

Complications of diabetes that contribute to the increased risk of foot problems and
infection include the following –

 Neuropathy – sensory neuropathy leads to loss of pain and pressure sensation,

and autonomic neuropathy leads to increased dryness and fissuring of the skin
(secondary to decreased sweating). Motor neuropathy results in muscular
atrophy, which may lead to changes in the shape of the foot.
 Peripheral vascular disease – poor circulation of the lower extremities
contribures to poor wound healing and the development of gangrene.
 Immunocompromise – hyperglycemia impairs the ability of specialized leukocytes
to destroy bacteria. Therefore, in poor control diabetes, there is a lowered
resistance to certain infections.
The sequence of events n the development of a diabetic foot ulcer begins with a soft
tissue injury of the foot, formation of a fissure between the toes or in an area of dry
skin, or formation of a callus. Patients with an insensitive foot do not feel injuries, which
may be thermal (eg. From using heating pads, walking barefoot on hot concrete, testing
bath water with the foot), chemical (eg. Burning of foot while using caustic agents on
calluses, corns, or bunions), or traumatic (eg. Injuring skin while cutting nails, walking
with an undetected foreign object in the shoe, or wearing ill-fitting shoes and socks).

Characteristics of patients having high risk of foot ulcer –

 Duration of diabetes more than 10 years

 Age older than 40 years
 History of smoking
 Decreased peripheral pulse
 Decreased sensation
 Anatomic deformities or pressure areas (eg. Bunions, calluses, hammer toes)
 History of previous foot ulcers or amputation

Management –

 Preventive foot care begins with carefully daily assessment of the feet, which
should be inspected on a daily basis for any redness, blisters, fissures, calluses,
ulcerations, changes in skin temperature, or development of foot deformities
(hammer toes, bunions). Visual impairement or decreased joint mobility
(specially in elderly) requires use of a mirror to inspect the bottoms of both feet
or the help of a family member in foot inspection. The interior surface of the
shoes should be inspected for any rough spots or foreign objects.
xxxvi
  Properly bathing, drying, and lubricating the feet, taking care not to allow
moisture (water or lotion) to accumulate between the toes.

 Wearing closed-toed shoes that fit well. Provide the patient with inserts to
remove pressure from pressure points on the foot. New shoes should be broken
in slowly (i.e, worn for 1 to 2 hours initially, with gradual increases in the length
of time worn) to avoid blister formation. Patient with bony deformities may need
custom-made shoes with extra width or depth. High risk behaviours, such as
walking barefoot, using heating pads on the feet, wearing open-toed shoes,
soaking the feet, and shaving calluses, should be avoided.

 Trimming toe nails straight across and filing sharp corners to follow the contour
of toe. If the patient has visual deficit, is unable to reach the feet because of
disability, or has thickened toenails, a podiatrist should cut the nails.

 Reducing risk factors, such as smoking and elevated blood lipids, that contribute
to peripheral vascular disease.

 Avoiding home remedies, over-the-counter agents, and self-medicating to treat

foot problems.

FOOT CARE TIPS –

1. Keep blood glucose level within a normal range.

2. Inspect feet everyday. Look at for cuts, blisters, red spots and swelling. Use mirror
to check the bottom of feet or ask family member for help, if any difficulty in
seeing. Check for changes in temperature.

3. Wash feet every day. wash feet in warm, not hot water. Dry feet well. Be sure to
dry between the toes. Do not soak feet. Donot check water temperature with
your feet, use a thermometer or elbow.

4. Keep skin soft and smooth. Rub lotion over the tops and bottom of feet, but not
between the toes.

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5. Smooth corns and calluses gently. Use a pumice stone to soft corns and calluses.

6. Trim toenails each week or when needed. Trim toenails straight across and file
the edges with an emery board or nail file.

7. Wear shoes and socks at all times. Never walk barefoot. Wear comfortable shoes
that fit well and protect feet. Feel inside the shoes before putting them on each
time to make sure the lining is smooth and there are no object to make sure the
lining is smooth and there are no objects inside.

8. Protect feet from hot and cold. Wear shoes at the beach or on hot pavement.
Waer socks at night if feet get cold.

9. Keep the blood flowing to feet. Put feet up when sitting. Wiggle toes and move
ankles up and down for 5 minutes, 2 or 3 times a day. donot cross legs for long
periods of time. Do not smoke.

10. Check with your health care provider –

 Have your health care provider check your bare fee and find out ehether
you are likely to have serious foot problems. Remember that you may not
feel the pain of an injury.
 Call your health care provider right away if a cut, sore, blister, or bruise on
your foot does not being to heal afler one day.
 Follow your health care provider’s advice about foot care.
 Donot self-medicate or use home remedies or over the counter agents to
treat foot problems.

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