Institute of Nursing

Dr. Nicanor Reyes St., Sampaloc Manila

S.Y. 2009 – 2010

In Partial Fulfillment
Of the Requirements
In NCM 104

CASE PRESENTATION
DEEP VEIN THROMBOSIS

Submitted by:
BSN127/GROUP107
Caraig, Jianina Marie
Lingcaso, Maria Consuelo
Mauricio, Justine Barbara
Mendoza, Joana Erica
Navasca, Irvin Angelo
Nivero, Joanne Carla
Olimba, Rachelle Joyce
Pagtama, Altini
Pantaleon, Mark Kevin
Pentecostes, Mary Lopeline
Portento, Erick Anthony
 Submitted to:
Ma’am Brenda Lambio,RN
Introduction to deep vein thrombosis (DVT)

Arteries have thin muscles within their walls to be able to withstand the
pressure of the heart pumping blood to the far reaches of the body. Veins
don't have a significant muscle lining, and there is nothing pumping blood
back to the heart except physiology. Blood returns to the heart because the
body's large muscles squeeze the veins as they contract in their normal
activity of moving the body. The normal activities of moving the body returns
the blood back to the heart.

There are two types of veins in the leg; superficial veins and deep veins.
Superficial veins lie just below the skin and are easily seen on the surface.
Deep veins, as their name implies, are located deep within the muscles of
the leg. Blood flows from the superficial veins into the deep venous system
through small perforator veins. Superficial and perforator veins have one-
way valves within them that allow blood to flow only in the direction of the
heart when the veins are squeezed.

A blood clot (thrombus) in the deep venous system of the leg is not
dangerous in itself. The situation becomes life-threatening when a piece of
the blood clot breaks off (embolus, pleural=emboli), travels downstream
through the heart into the pulmonary circulation system, and becomes
lodged in the lung. Diagnosis and treatment of a deep venous thrombosis
(DVT) is meant to prevent pulmonary embolism.

Clots in the superficial veins do not pose a danger of causing pulmonary

emboli because the perforator vein valves act as a sieve to prevent clots
from entering the deep venous system. They are
usually not at risk of causing pulmonary
embolism.

What are the causes of deep vein thrombosis?

Blood is meant to flow; if it becomes stagnant

there is a potential for it to clot. The blood in veins
is constantly forming microscopic clots that are
routinely broken down by the body. If the balance
of clot formation and resolution is altered,
significant clotting can occur. A thrombus can form if one, or a combination
of the following situations is present.
Immobility

• Prolonged travel and sitting, such as long airplane flights ("economy

class syndrome"), car, or train travel
• Hospitalization
• Surgery
• Trauma to the lower leg with or without surgery or casting
• Pregnancy, including 6-8 weeks post partum
• Obesity

Hypercoagulability (coagulation of blood faster than usual)

• Medications (for example, birth control pills, estrogen)

• Smoking
• Genetic predisposition
• Polycythemia (increased number of red blood cells)
• Cancer

Trauma to the vein

• Fracture to the leg

• Bruised leg
• Complication of an invasive procedure of the vein

What are the symptoms of deep vein thrombosis?

Superficial thrombophlebitis

Blood clots in the superficial vein system most often occur due to trauma to
the vein which causes a small blood clot to form. Inflammation of the vein
and surrounding skin causes the symptoms of any other type of
inflammation including:

• redness,
• warmth,
• tenderness, and
• swelling.

Often the affected vein can be palpated (felt) as a firm, thickened cord.
There may be inflammation that follows the course of part of the vein.

Although there is inflammation, there is no infection.

Varicosities can predispose to superficial thrombophlebitis. When the valves

of the larger veins in the superficial system fail (the greater and lesser
saphenous veins), blood can back up and cause the veins to swell and
become distorted or tortuous. The valves fail when veins lose their elasticity
and stretch. This can be due to age, prolonged standing, obesity, pregnancy,
and genetic factors.

Deep Venous Thrombosis

The symptoms of deep vein thrombosis are related to obstruction of blood

returning to the heart and causing a backup of blood in the leg. Classically,
they symptoms include:

• pain,
• swelling,
• warmth, and
• redness.

Not all of these symptoms have to occur; one, all, or none may be present
with a deep vein thrombosis. The symptoms may mimic an infection or
cellulitis of the leg.

Historically, healthcare providers would try to elicit a couple of clinical

findings to make a diagnosis. Dorsiflexion of the foot (pulling the toes
towards the nose, or Homans' sign) and Pratt's sign (squeezing the calf to
produce pain), have not been found effective in making a diagnosis.

When should I seek medical care for deep vein thrombosis?

The diagnosis of a superficial or deep thrombosis often relies on the clinical

skill of the health care practitioner. Diagnostic tests need to be tailored to
each situation.

Leg swelling, redness, and pain may be indicators of a blood clot and should
not be ignored. These symptoms may be due to other causes (for example,
cellulitis or infection), but it may be difficult to make the diagnosis without
seeking medical advice.

If there is associated chest pain or shortness of breath, then further concern

exists that a pulmonary embolus may be the cause. Once again, seeking
immediate advice is appropriate.

How is deep vein thrombosis diagnosed?

The diagnosis of superficial thrombophlebitis is made clinically.

Ultrasound is now the standard method of diagnosing the presence of a deep

vein thrombosis. The ultrasound technician may be able to determine
whether a clot exists, where it is located in the leg, and how large it is.
Ultrasounds can be compared over time to see whether a clot has grown or
resolved. Ultrasound is better at "seeing" veins above the knee as compared
to the veins below it.

Venography, injecting dye into the veins to look for a thrombus, is not
usually performed any more and has become more of a historical footnote.

D-dimer is a blood test that may be used as a screening test to determine if

a blood clot exists. D-dimer is a chemical that is produced when a blood clot
in the body gradually dissolves. The test is used as a positive or negative
indicator. If the result is negative, then no blood clot exists. If the D-dimer
test is positive, it does not necessarily mean that a deep vein thrombosis is
present since many situations will have an expected positive result (for
example, from surgery, a fall, or pregnancy). For that reason, D-dimer testing
must be used selectively.

Other blood testing may be considered based on the potential cause for the
deep vein thrombosis.

What is the treatment for deep vein thrombosis?

Superficial Thrombophlebitis

Treatment for superficial blood clots is symptomatic with:

• warm compresses,
• leg compression, and
• an anti-inflammatory medications such as ibuprofen.

If the thrombophlebitis occurs near the groin where the superficial and deep
systems join together, there is potential that the thrombus could extend into
the deep venous system. These patients may require anticoagulation or
blood thinning therapy (see below).

Deep venous thromboses

Deep venous thromboses that occur below the knee tend not to embolize
(break loose). They may be observed with serial ultrasounds to make certain
they are not extending above the knee. At the same time, the cause of the
deep vein thrombosis may need to be addressed.

The treatment for deep venous thrombosis above the knee is

anticoagulation, unless a contraindication exists. Contraindications include
recent major surgery (since anticoagulation would thin all the blood in the
body, not just that in the leg, leading to significant bleeding issues), or
abnormal reactions when previously exposed to blood thinner medications.

Anticoagulation prevents further growth of the blood clot and prevents it

from forming an embolus that can travel to the lung.

Anticoagulation is a two step process. Warfarin (Coumadin) is the drug of

choice for anti-coagulation. It is begun immediately, but unfortunately it may
take a week or more for the blood to be appropriately thinned. Therefore,
low molecular weight heparin [enoxaparin (Lovenox)] is administered at the
same time. It thins the blood via a different mechanism and is used as a
bridge therapy until the warfarin has reached its therapeutic level.
Enoxaparin injections can be given on an outpatient basis.

For those patients who have contraindications to the use of enoxaparin (for
example, kidney failure does not allow the drug to be metabolized),
intravenous heparin can be used as the first step. This requires admission to
the hospital.

The dosage of warfarin is monitored by blood tests measuring the

prothrombin time or INR (international normalized ratio). For an
uncomplicated deep vein thrombosis, the recommended length of therapy
with warfarin is three to six months.

Some patients may have contraindications for warfarin therapy, for example
a patient with bleeding in the brain, major trauma, or recent significant
surgery. An alternative may be to place a filter in the inferior vena cava (the
major vein that collects blood from both legs) to prevent emboli from
reaching the heart and lungs. These filters may be effective but also may be
the source of new clot formation.

Surgery

Surgery is a rare option in treating large deep venous thrombosis of the leg
in patients who cannot take blood thinners or who have developed recurrent
blood clots while on anti-coagulant medications. The surgery is usually
accompanied by placing an IVC (inferior vena cava) filter to prevent future
clots from embolizing to the lung.

Phlegmasia Cerulea Dolens describes a situation in which a blood clot forms

in the iliac vein of the pelvis and the femoral vein of the leg, obstructing
almost all blood return and compromising blood supply to the leg. In this
case surgery may be considered to remove the clot, but the patient will also
require anti-coagulant medications.
What are the complications of deep vein thrombosis?

Pulmonary embolism is the major complication of deep vein thrombosis. It

can present with chest pain and shortness of breath and is a life-threatening
condition. More than 90% of pulmonary emboli arise from the legs.

Post-phlebitic syndrome can occur after a deep vein thrombosis. The

affected leg can become chronically swollen and painful with skin color
changes and ulcer formation around the foot and ankle.

Can deep vein thrombosis be prevented?

As is the case with most medical illnesses, prevention is of prime

importance. Minimizing risk factors is key to deep vein thrombosis
prevention.

In the hospital setting, the staff works hard to minimize the potential for clot
formation in immobilized patients. Compression stockings are routinely used.
Surgery patients are out of bed walking (ambulatory) earlier and low dose
heparin or enoxaparin is being used for deep vein thrombosis prophylaxis
(measures taken to prevent DVT).
For those who travel, it is recommended that they get up and walk every
couple of hours during a long trip. Compression stockings may be helpful in
preventing future deep vein thrombosis formation in patients with a previous
history of a clot.
I. BIOGRAPHIC DATA

The client named M.S., a 64 year old female, living at 178 Brgy.
C, Rosario, Batangas Phil. 4225. She was born at Pangasinan on
March 13, 1946. Her nationality is Filipino, she is a Roman Catholic.
Her highest educational attainment is Grade 6 same with her
husband, N. S. Jr. She has 3 children; all are college graduates with
degrees and is now working abroad with their own family.

NURSING HISTORY

A. PAST HEALTH HISTORY

 The client had 15 years of going in and out of the hospital
due to vomiting, but with no serious diagnosis. She has no known
allergies to foods and medicines. The patient had Diabetes type
2 for almost 15 years now with some medications taken:
Allopurinol, Vitamin B complex, Iberet, Rosuvastatin and
Irbesartan. She has no history of travel in the past years.

B. HISTORY OF PRESENT ILLNESS

3 weeks prior to admission, the patient noted bipedal

edema with associated marginal urine output. No DOB/SOB,
chest pain. Palpitations and orthopnea noted. No medications
were taken. Persistence prompted consult with AMP hence this
admission. The client has been diagnosed of having DVT, DM
type II, Diabetic kidney disease, dyslipidemia, HCVD. Her
attending physician, Dr. Montano prescribed: Burinex, Arixtra,
Coumadin, Kalimate, Serokot, Himulin R, Neurontin and Crestor.

The client complains of feeling of numbness in her both

feet, when asked if the client feels pain, the client verbalized “
masakit ang paa ko pag nagagalaw, o kaya ay napipisil, lalo na
pag naglalakad ako.”

When both feet are palpated with light pressure added

facial grimace were noted.

The client rate her pain 6/10 as 10 being the highest and 1
being the lowest.

C. FAMILY HISTORY
 The patient stated that her mother is diabetic and died
because of the disease, while her father died when she was still
young. Diabetes and hypertension are prominent in their family.

II. PATTERNS OF FUNCTIONING

A. PSYCHOLOGICAL HEALTH

The client described a stressful event as: “hindi na

nagagawa yung mga dating nagagawa, hindi na
makapagtrabaho tulad ng dati” According to her, she usually
cries whenever problems come her way, she verbalized; “pag
may problema, naiyak lang ako tapos wala na, okay na ulit. Ang
hipag at asawa ko ang madalas na kausap ko” The patient is not
having problem regards to her family, she stated “wala akong
problema sa asawa ko, yung mga anak ko naman puro mga
nasa abroad, yung mga kasama ko lang sa bahay and di ko
nakakasundo paminsan.” “pinaguusapan lang namin ang di
pagkakasundo,tapos okay na”. The patient rated her health
status as 5/10, as 10 being the highest, she verbalized; “5 kasi di
pa nawawala ang manas ko pag nawala na, tsaka tataas.” When
asked about her sexual activity, she answered; “naku,di na kami
nagtatabi nun, magkahiwalay kami ng kama at ayaw nya na
nagdidikit kami, babaero kasi yun dati. At nagpavasectomy na
rin sya pagkatapos ng huli naming anak.” She rated her self-
esteem as 8/10, as 10 being the highest because despite the
stressors that come her way, she is fulfilled since she was able to
send her children to school and manage to let them finish and all
of them are successful.
CUES ANALYSIS/ INTERPRETATION

Analysis: Stress can have

physical, emotional,
“pag may problema, naiyak
intellectual, social, and spiritual
lang ako tapos wala na, okay
consequences. Usually the
na ulit. Ang hipag at asawa ko
effects are mixed, because
ang madalas na kausap ko”
stress affects the whole person.
client verbalized.
Physically, stress can threaten
The client described a stressful a person’s physiologic
event as: “hindi na nagagawa homeostasis. Emotionally,
yung mga dating nagagawa, stress can produce negative or
hindi na makapagtrabaho tulad non constructive feelings about
ng dati” the self. Intellectually, stress
can influence a person’s
The patient rated her health
perceptual and problem-solving
status as 5/10, as 10 being the
activities. Socially, stress can
highest , she verbalized; “5
alter a person’s relationships
kasi di pa nawawala ang manas
with others. Spiritually, stress
ko pag nawala na, tsaka
can challenge one’s beliefs and
tataas.”
values.

Interpretation: The client is

handling her stress by talking
to her spouse and sister-in-law
with regards to her concerns
and problems, and at the same
time releasing it through
crying.
 Fundamentals of Nursing 8th
Edition Volume 2 page 1061

A. SOCIOCULTURAL PATTERNS

The patient doesn’t have regular exercise, when asked

about the usual thing she does when at home, she answered;
“nakahiga lang, nuod ng tv, di na kasi ako makalakad ng
matagal, at masakit ang paa ko.” The client owns a small
canteen in their home in Rosario, Batangas from where they get
their income, but due to financial constraint, they cannot afford
to do the angiogram procedure to detect where the exact
location of the thrombus that causes the clients’ DVT. She
described the environment near their house as; “2 storey ang
bahay, 3 kwarto sa itaas at 1 sa ibaba, sa labas naming ang
kainan, katabi ang highway kaya talagang mausok, at
maalikabok.”

CUES ANALYSIS/INTERPRETATION

The patient doesn’t have Client’s Exercise

regular exercise, when asked
• Exercises that exercise
about the usual thing she large muscle groups
does when at home, she rhythmically, such as
walking, are good.
answered; “nakahiga lang,
nuod ng tv, din na kasi ako (Maternal & Child Health Nursing:
makalagad ng matagal, at Care of the Childbearing &
ansakit ng paa ko.” Childrearing Family, 5th edition,
Volume 1, page 276, Pillitteri)
She described the
environment near their house
Interpretation
as; “2 storey ang bahay, 3
kwarto sa itaas at 1 sa ibaba, Due to her illnesses the client
sa labas naming ang kainan, wasn’t able to perform exercises;
katabi ang highway kaya strenuous activities will cause
talagang mausok, at more pain to the client.
maalikabok.”

A. SPIRITUAL PATTERNS

The client is a Roman Catholic, she is not able to attend

mass since she is already having a hard time walking and easily
gets tired, but according to her; “kahit di ako nakakapag simba,
may sarili ako paraan para magdasal, sa bahay lang, diretso na
sa kanya.”

CUES ANALYSIS/ INTERPRETATION

“kahit di ako nakakapag Analysis: Religion is an

simba, may sarili ako paraan organized beliefs and practices.
para magdasal, sa bahay lang, It offers a way of spiritual
diretso na sa kanya.” Client expression that provides
stated guidance for believers in
responding to life’s questions
and challenges. (Kozier p. 996)

People nurture or enhance

their spirituality in many
ways. Some focus on
development of the inner
 self or world; others focus
on the expression of their
spiritual energy with
others or outer world.

Kozier 7th Ed. p. 996

Interpretation:

Despite the fact that client can

no longer attend Sunday Mass,
she still able to maintain her
faith to God in her personal
ways.

I. ACTIVITIES OF DAILY LIVING

 ADL BEFORE AFTER INTERPRETATI
HOSPITALIZAT HOSPITALIZAT ON AND
ION ION ANALYSIS

V. PHYSICAL 1. NUTRITION “madalas Client’s diet is Client’s food

intake:
ASSESSMENT barbeque, now controlled
salad, cake, and usually eats • Client is
taba ng baboy a DM diet. She not able
to adhere
at gulay” she now drinks to a to her
usually drinks 1liter of water in physician’
s advice.
3liters of water 24 hours.
in 24 hours. • Her food
choices,
which are
precipitati
ng
factors,
may pose
as a
predisposi
ng factor
of her
illness

(Patricia
Skinner (2001),
Unani-tibbi,
Encyclopedia of
Alternative
Medicine)
2. ELIMINATION He urinates 10 She urinates the Client’s
intestinal
times in a day same amount
elimination:
with yellowish and has the • There is
color and same no exact
frequency
odorless. She characteristics. of bowel
defecates thrice movemen
t
 • Weight: 90kg. (198 lbs.) Obese Class II (BMI = 36.6)
• Height: 66 inches.
• BP: 130/90
• RR: 20cpm
• PR: 82bpm

A. Physical Assessment

Area to be Assessed Normal Findings Actual Findings Interpretation

1. General Appearance
a. Mood and Affect Appropriate to situation Appropriate to situation Normal

b. Signs of Distress No distress noted No Distress noted Normal

c. Posture Erect posture Slouched Abnormal
d. Body movement Coordinated movement Slow movement Normal
e. Hygiene and Clean and neat Clean and neat Normal
Grooming

f. Type of Clothing Neat and appropriate Neat and appropriate Normal

2. Head to Toe
Examination
Integumentary System
a. Skin The color varies light to Uniform fair complexion Abnormal
dark brown generally except those areas
uniform except in areas exposed to sun. Grade 1
exposed to the sun. No bipedal edema
edema, no Lesions. Skin
turgor is normal.
b. Nails About 160 degrees, Nails in hands are convex Normal
convex curvature curvature, with nail
polish on fingernails, toes
on nails are triangular.

Head
a. Skull Proportional to the size of Proportional to the size of Normal
the body the body
Absence of nodules and Absence of nodules and
muscles muscles
b. Scalp White, clean, free from Clean Normal
dandruff, and lesions No dandruff
No areas of tenderness No lesions
No tenderness
c. Hair Evenly distributed Evenly distributed Normal
Short and wavy black
hair
No presence of head
lice
d. Face Symmetrical facial Symmetrical Normal
features and movements
e. Eyebrows Symmetrical Symmetrical Normal
Evenly distributed Evenly distributed
f. Eyelashes Evenly distributed Evenly distributed Normal
Curled outward Curled outward
g. Eyelids Cover a small portion of Slightly-covered small Normal
iris, cornea, and sclera portion of iris, cornea,
and sclera
h. Conjunctiva Transparent, shiny, Transparent, shiny, Normal
smooth, pink in color moist, pinkish in color

I. Sclera White and clear White and clear Normal

Some capillaries and
veins are visible
j. Cornea Transparent, shiny and Transparent, shiny and Normal
smooth smooth
k. Iris Visible, round, flat Visible, round, flat Normal
surface surface, brown in color
l. Pupil Black, round, Black, round, Normal
symmetrical symmetrical
m. Eye Movement Coordinated eye Coordinated Normal
movement
n. Visual Acuity 20/20 vision Cannot read newsprints. Abnormal
Has astigmatism
p. Ears Symmetrical, auricles are Symmetrical, Normal
aligned with the outer Auricles are aligned with
cantus of the eye the outer cantus of the Normal
No lesions and blood eye
Ear Canal No presence of blood and
lesions
q. Nose Normal
Internal Nares No swelling or discharge No swelling or discharge
Midline, straight Midline, straight
s. Mouth Pinkish, symmetrical, Pinkish, Normal
Lips moist
Gums Pinkish, moist, firm Pinkish, moist
Teeth texture
Tongue 32 sets of teeth Using dentures
Frenulum smooth, no palpable Pinkish, no lesions Abnormal
Buccal Mucosa nodules, pinkish
Palate no lesions Midline position, pinkish
Uvula moist, no lesions and moist
Tonsils pinkish, moist
position in midline

Neck
a. Lymph Nodes Not palpable, no Not palpable, no Normal
tenderness tenderness
b. Trachea Central placement in the Central placement in the Normal
midline of the neck midline of the neck
c. Thyroid Gland Ascends during Ascends during Normal
swallowing, small, swallowing, small,
smooth smooth
d. Muscle Strength Client was able to resist Not able to resist force Normal
the force
Thorax
a. Posterior Thorax Anteroposterior thorax to Anteroposterior thorax to Normal
transverse diameter is in transverse diameter is in
ratio of 1:2 ratio of 1:2
Full symmetric chest Full symmetric chest
expansion expansion
Uniform in color Uniform in color
No tenderness No tenderness
b. Anterior Thorax Quiet, effortless Full symmetric expansion Normal
respiration Uniform in temperature
Bronchial breath sounds No tenderness
Uniform temperature Full symmetric expansion
No tenderness No Presence of Rales
Full symmetric expansion (crackles) breath sounds

c. Cardiovascular No pulsation except for No pulsation except for Normal

Aortic Aortic
No lift or heave No lift or heave
d. Carotid Arteries Symmetric pulse, volume Symmetric pulse volume Normal
No sounds heard No sounds heard
e. Jugular Veins Veins are not visible Veins are not visible Normal

Breast
a. Areola Round, same color varies Round, same color varies Normal
widely widely
No positive masses or No positive masses or
lesions lesions
Pinkish in color
b. Nipple Round, everted, equal in Round, everted, equal in Normal
size size
Both nipples are in Both nipples are in the
similar direction same direction
Has no discharge and no Has no discharge and no
lesions lesions
Abdomen Uniform in color Normal
Flat, rounded, symmetric Uniform in color, round
contour, and no evidence and soft abdomen
of enlargement of liver or
spleen
No tenderness
Musculoskeletal
System
a. Muscles Equal sides of the body Equal sides of the body Normal
No fasciculation and No fasciculation and
tremors tremors
Normally firm Normally firm
b. Upper and Lower Client was able to resist Lower wasn’t able to Abnormal
Extremities the force resist the force because
of pain, Grade 1 bipedal
edema
c. Bones No deformities, No deformities, Normal
tenderness, or swelling tenderness, or swelling
d. Joints No swelling, tenderness, No swelling, Tenderness, Normal
Moves smoothly Moves smoothly
ECOLOGIC
MODEL

A.

Hypothesis

Deep vein thrombosis (DVT) is a condition in which a blood clot

(thrombus) forms in one or more of the deep veins in your body, usually in
your legs. Deep vein thrombosis can cause leg pain, but often occurs
without any symptoms. Deep vein thrombosis is a serious condition
because a blood clot that has formed in your vein can break loose and
travel to your lungs.
In the case of our patient, she has DVT at her left proximal to mid
posterior tibial vein. This is probably due to her disease (Diabetes
Mellitus), and her lifestyle. She don’t exercise and she is obese.
B. Pre-disposing Factors

• Diabetes Mellitus

• Sex

• Obesity

• Lifestyle

• Age
C. Analysis

Virchow's triad is a group of three factors known to affect clot formation:

rate of flow, the consistency (thickness) of the blood, and qualities of the
vessel wall. Virchow noted that more deep venous thrombosis occurred in
the left leg than in the right and proposed compression of the left common
iliac vein by the overlying right common iliac artery as the underlying cause
• Sitting for long periods of time, such as when driving or
flying. When your legs remain still for long periods, your calf muscles
don't contract, which normally helps blood circulate. Blood clots can
form in the calves of your legs if your calf muscles aren't moving.
Although sitting for long periods is a risk factor, your chance of
developing deep vein thrombosis while flying or driving is relatively
low.

• Prolonged bed rest, such as during a long hospital stay, or

paralysis. When your legs remain still for long periods, your calf
muscles don't contract to help blood circulate, which can make blood
clots develop.

• Being overweight or obese. Being overweight increases the

pressure in the veins in your pelvis and legs.

• Sex. Pregnancy. Pregnancy increases the pressure in the veins in

your pelvis and legs. Women with an inherited clotting disorder are
especially at risk. The risk of blood clots from pregnancy can continue
for up to six weeks after you have your baby.

D. Conclusion
 We therefore conclude that our client is suffering from Deep Vein
thrombosis is probably due to her lifestyle, her disease. Other risk factors
may also involve such as age and the way of living.

A. Hypothesis
Diabetes Mellitus is a condition in which the pancreas can no
longer produces enough insulin or cells stop responding to the insulin that is
produced, so that glucose in the blood cannot be absorbed in the ells of the
body.
In the case of our patient, the form of diabetes she has is Type
2; it sometimes called age-onset or adult- onset diabetes. This is probably
due to her lifestyle. She is fond of eating salad, cake pork fats,
environmental factors may also involve. The clients’ relatives also have this
illness, which the family or genetic history of diabetes play a role in the
occurrence of diabetes mellitus.

B. Pre-disposing Factors

•Host
-female
-64 years old
-sedentary lifestyle
-family history of diabetes
-diet
• Agent
-chemical- glucose (and any type of sugar)

•Environment
-living conditions
-economic level

Host
-female
-64 years old
-sedentary lifestyle
-family history of diabetes
-diet

Environme
nt
 -living conditions
-economic level
Agent
-chemical-
glucose

C. Analysis
The agent-host-environment model is primarily use in predicting
illness rather than promoting wellness, although identification of risk factors
that result from the interactions of agent, host, and environment are helpful
in promoting and maintaining health. Because each of the agent-host-
environment factors constantly interacts with others, health is an ever
changing state. Health is seen when all three elements are in balance while
illness is seen when one, two, or all three elements are not in balance
(Fundamentals of Nursing by Kozier 2004)

Diabetes Mellitus is a group of metabolic diseases characterized

byelevated levels of glucose in the blood (hyperglycemia) resulting from
defects in insulinsecretions, insulin action or both. Insulin controls the level
of glucose in the blood byregulating the production and storage of glucose.
In the diabetic state, the cells maystop responding to insulin or the pancreas
may stop producing insulin entirely.
(Fundamentals of Nursing by Taylor)

Diabetes Mellitus is disorder, when we eat; most of the food we

eat isbroken down by digestive juices into chemicals. Type 2 diabetes
mellitus- these clientshave insulin resistance with relative deficiency. Ages,
lack of exercise, history of GDM,hypertension, dyslipidemia are all risk
factors.
(Medical- Surgical Nursing by Lois White.pg.698)

D. Conclusion
We therefore conclude that our client is suffering from Type 2
Diabetes Mellitus. Probably due to her lifestyle before and having a family
history of the disease. Other risk factors may also involve such as age and
the way of living.

E. Management
Medical Management:
 -oral hypoglycemic Agents
E.g. SULFONYLUREA, GLIPZIDE, METFORMIN

Nursing Management:
•dietary mngt.-Nutritional Therapy
-provide adequate calories to maintain a reasonable
weight.

•Exercise
-to maintain weight.
-lowering blood glucose
-increase circulation
-improves cardiovascular status
-decreases stress
•Monitoring glucose level and urine for ketones
•Maintain skin integrity by protecting feet from breakdown
•Health promotion
-assisting the client and family to understand diabetes
and the necessary
lifestyle changes.

DISCUSSION OF THE ANATOMY INVOLVED

PANCREAS
The pancreas is located retroperitoneal, posterior to the stomach in the
inferior part of the left upper quadrant. The right side of the organ (called the
head) is the widest part of the organ and lies in the curve of the duodenum
(the first section of the small intestine). The tapered left side extends slightly
upward (called the body of the pancreas) and ends near the spleen (called
the tail).
The pancreas in an organ that contains two basic types of tissue: the
acini, which produce digestive enzymes, and the islets, which produce
hormones (insulin and glucagon). The pancreas secretes digestive enzymes
into the duodenum and hormones into the bloodstream.
The digestive enzymes are released from the cells of the acini and flow down
various channels into the pancreatic duct. The pancreatic duct joins the
common blie duct at the sphincter of Oddi, where both flow into the
duodenum.
The enzymes secreted by the pancreas digest proteins, carbohydrates, and
fats. The proteolytic (protein-digesting) enzymes, which break down proteins
into a form that the body can use, are secreted in an inactive form. The
pancreas also secretes large amount of sodium bicarbonate, which protects
the duodenum by neutralizing the acid (chyme) that comes from the
stomach.
The three hormones produced by the pancreas are insulin, which lowers the
level of sugar (glucose) in the blood; glucagon, which raises the level of
sugar in the blood; and somatostatin. Which prevents the other two hormone
from being released.

VEINS
The veins return blood to the heart from all the organs of the body. The
legs contain two major group of veins: the superficial veins, located in the
fatty layer under the skin, and the deep veins, located in the muscles.
Blood has to flow from the leg veins upward to reach the heart when a
person is standing. The deep veins play a major role in propelling blood
upward. Located within the powerful calf muscles, these veins are forcefully
compressed with every step.
To keep the blood flowing up, not
down, the deep veins contain one-
way valves. Each valve consists of
two halves (cusps) with edges that
meet. The blood pushes the cusps
open like a pair of swinging doors,
but blood forced in the opposite
direction by gravity pushes the
cusps closed.

Superficial veins have the

same type of valves, but these
veins don’t get squeezed because
they aren’t surrounded by muscles. So blood in the superficial veins flows
more slowly than blood in the deep veins. Much of the blood that flows up
the superficial veins is diverted into the deep veins through the many short
veins that connect the two systems.

Deep Vein Thrombosis

PATHOPHYSIOLOGY
Pre-disposing Factors Precipitating Factors
-female -Sedentary Lifestyle
-Diet
-Obesity
-64 years old
-family history of diabetes
-Family hx of HPN

Diabetes
Immobility
Mellitus

Hypercoagubi
lity

Blood pools by
gravity in the Elevated Coagulation
veins markers & Plasma
level of clotting
factors

Platelets & Fibrin

form the initial clot

RBC are trapped

in the fibrin
meshwork

Thrombus
Propagates in the
direction of blood

Inflammation is
triggered

Causes Inflammation,
swelling & erythema
LABORATORY RESULTS
RIGHT LEFT
PSV(cm/s WAVEFORM PSV(cm/s WAVEFORM
ec) ec)
Distal Internal 166 TRIPHASIC 220 TRIPHASIC
Iliac(DEIA)
Common 131 TRIPHASIC 184 TRIPHASIC
Femoral(CFA)
Deep 172 TRIPHASIC 204 TRIPHASIC
Profunda(DFA)
Superficial
Femoral(SFA)
Proximal 196 TRIPHASIC 366 TRIPHASIC
Mid 270 TRIPHASIC 152 TRIPHASIC
Distal 213 TRIPHASIC 208 TRIPHASIC
Popliteal(PA)
Proximal 140 TRIPHASIC 189 TRIPHASIC
Mid 104 TRIPHASIC 98 TRIPHASIC
Distal 123 TRIPHASIC 130 TRIPHASIC
Tibio peroneal 104 TRIPHASIC 120 TRIPHASIC
Trunk(TPT)
Peroneal(PeA) 177 TRIPHASIC 116 TRIPHASIC
Posterior
Tibial(PTA)
Proximal 98 TRIPHASIC 130 TRIPHASIC
Mid 187 TRIPHASIC 46 TRIPHASIC
Distal 98 TRIPHASIC 57 TRIPHASIC
Anterior Tibial
Proximal 93 TRIPHASIC 68 TRIPHASIC
Mid 49 TRIPHASIC 44 TRIPHASIC
Distal 72 TRIPHASIC 34 TRIPHASIC
Dorsalis pedis(DPA) 19 TRIPHASIC 70 TRIPHASIC

Comments:
B-mode imaging should diffuse intimal thickening with calcified plaque
formation along the anterior and posterior wall of all arterial segments of the
bilateral lower extremities.
Interpretation:
Lower extremities atherosclerotic arterial disease with:
• 20- 49% stenosis, Right common femoral artery and mid to distal
superficial artery.
 Left distal external iliac artery, profunda femoris artery,
proximal superficial femoral artery and proximal to distal
Doppler Distal Comm Femor Poplite Tibio Anteri Posteri Perone Greater Lesser Sapheno Sapheno
signal Extern on al al Perone or or al Sapheno Sapheno us us
al Iliac Femor al Tibial tibial us us Femoral Popliteal
al Junction Junction
Compresibi R L R L R L R L R L R L R L R L R L R L R L R L
lity
Spontaneo F F F F F F F F F F F F F F F F F F F F F F F F
us
Phasic + + + + + + + + + + + + + + + + + + + + + + + +
Augmented + + + + + + + + + + + + + + + + + + + + + + + +
Competent + + + + + + + + + + + + + + + + + + + + + + + +
Nonpulsatil + O + O + + + + + + + O + P + O O O O + O O + +
e
+ + + + + + + + + + + + + + + + + + + + + + + +
popliteal artery.

• 1-19% stenosis, the rest of the arterial segments.

VENOUS DUPLEX SCAN LOWER EXTRIMITIES

LEGEND:
+ Present
O Absent
C Continuous
F Fully
P Partial

Venous Compression Result:

Comments:
The Left proximal to mid posterior tibial vein is partially compressible, dilated
containing a hypoechoic intraluminal density with partial color flow signal.

Conclusion and Recommendation:

• Deep vein thrombosis, acute, partially occluding the Left proximal to
mid posterior tibial vein.

• Deep vein valve incompetence: Right popliteal Vein, left common

femoral vein, anterior tibial vein, posterior tibial vein, peroneal vein.
 • Superficial vein valve incompetence: Bilateral greater saphenous vein
and Right lesser saphenous vein.

• Valve incompetence: Bilateral sapheno femoral junction

• Venous stasis: Bilateral lower extremities

• Tissue Edema: Bilateral Lower extremities

• Non thrombosed varicosities: Bilateral thigh, calf and ankle

• Incidental findings of Right popliteal cyst (1.2 x 4.1 cm)

URINE FLOW CYTOMETRY

Physical
RESULT NORMAL INTERPRETATION

Color Yellow Pale to Dark NORMAL

Yellow
Many foods and medicines can affect the
color of the urine. Urine with no color may
be caused by long-term kidney disease or
uncontrolled diabetes. Dark yellow urine
can be caused by dehydration. Red urine
can be caused by blood in the urine.

CLARITY Slightly Clear ABNORMAL

turbid
Cloudy urine can be caused by pus (white
blood cells), blood (red blood cells), sperm,
bacteria, yeast, crystals, mucus, or a
parasite infection, such as trichomoniasis.

Microscopic
TEST RESULT REFERENCE INTERPRETATION
VALUE
White Blood 1 0 – 4/hpf NORMAL
Cell
White blood cells (or leukocytes) in the
urine may be detected in the microscopic
analysis of urine. In general, the presence
of these cells in the urine is suspicious for a
urinary tract infection (UTI). Other
supportive evidence of a UTI may include
bacteria in the urine, leukocyte esterase
and nitrite on the dipstick, and clinical
evidence of urinary tract infection.

Red blood cell 3 0 – 4/hpf NORMAL

The presence of intact red blood cells in

the urine usually signifies a source of blood
loss in the lower part of the urinary tract
(urethra, bladder, ureters). Blood in the
urine may be visible by the naked eye
(gross hematuria) or only under the
microscope (microscopic hematuria). Gross
hematuria may be related to trauma to the
bladder or urethra, bladder tumors, or
hemorrhage.
Microscopic hematuria (red blood cells
seen only under microscope) may indicate
an infection in the lower urinary tract or a
kidney stone. Sometimes, red blood cells
may be seen in the form of red blood cell
casts, and this generally points to the
kidney as the source, such as an
inflammation of the kidney
(glomerulonephritis)..

Bacteria 396 0 – 1000/hpf NORMAL

Urine actually has little bacteria to begin

with. A lot of the filtrate are salts, water
and food pigments that pass through the
blood stream. If the person is sick, there
could be some of the bacteria that caused
the illness in urine. Urine accumulates
bacteria very fast.
A common way for urine to contract
bacteria is when it is kept in an infected
 bladder, which provides a fertile
environment for bacteria to grow. Bacteria
is the main cause of urinary tract
infections. When a large concentration of
bacteria is in the urine, it also could result
in Asymptomatic bacteriuria, a harmless
condition that often requires no treatment.

Epithilial cells 0 0 – 1/hpf NORMAL

The urinary tract is also lined with
epithelial tissues and so, it is normal to find
some of these cells in the urine. These cells
are detected in the urine during
microscopic urinalysis. However, the exact
quantity of the cells is identified during the
microscopic analysis of the urine sediment,
which is often done as the last step of the
urinalysis.

Cast 0 0 – 1/hpf NORMAL

The presence of cellular casts (casts

containing RBCs, WBCs, or epithelial cells)
identifies the kidneys, rather than the
lower urinary tract, as the source of such
cells. Cellular casts and renal epithelial
(kidney lining) cells are signs of kidney
disease.

Chemical
TEST RESULT NORMAL INTERPRETATION

Glucose NONE NONE NORMAL

Intravenous (IV) fluids can cause glucose to

be in the urine. Too much glucose in the
urine may be caused by uncontrolled
diabetes, an adrenal gland problem, liver
damage, brain injury, certain types of
poisoning, and some types of kidney
diseases. Healthy pregnant women can
have glucose in their urine, which is normal
 during pregnancy.

pH 5.5 4.6 - 8 UNHEALTHY

 Urine with a high pH can be an

indication of a urinary tract obstruction,
pyloric stenosis, urinary tract infection,
kidney failure and aspirin overdose.

 Generally, when urine pH is 6.0 and

below for extended periods of time, it is
an indication that the body's fluids
elsewhere are too acid, and it is working
overtime to rid itself of an acid medium.

Protein +++ Negative ABNORMAL

 Increase in serum total protein reflects

increases in albumin, globulin, or both.
Generally significantly increased total
protein is seen in volume contraction,
venous stasis, or in
hypergammaglobulinemia.

 Decrease in serum total protein reflects

decreases in albumin, globulin or both

Specific 1.015 1.010 – 1.020 NORMAL

Gravity
 A very high specific gravity means very
concentrated urine, which may be
caused by not drinking enough fluid,
loss of too much fluid (excessive
vomiting, sweating, or diarrhea), or
substances (such as sugar or protein) in
the urine.

 Very low specific gravity means dilute

urine, which may be caused by drinking
too much fluid, severe kidney disease,
or the use of diuretics.

Leukocyte NEGATIVE Negative NORMAL

 White blood cells (or leukocytes) in the
urine may be detected in the microscopic
analysis of urine. In general, the presence
of these cells in the urine is suspicious for a
urinary tract infection (UTI). Other
supportive evidence of a UTI may include
bacteria in the urine, leukocyte esterase
and nitrite on the dipstick, and clinical
evidence of urinary tract infection.

Nitrite NEGATIVE Negative NORMAL

Whereas nitrates are more or less normal

in urine (mainly coming from food
additives and from food protein, it seems,
though their origin is the subject to
extensive studies), the presence of
NITRITES IS NOT NORMAL.
Bacteria that cause a urinary tract infection
(UTI) produce an enzyme that converts
urinary nitrates to nitrites. The presence of
nitrites in urine indicates therefore a UTI
(urinary tract infection). Urinary tract
infections are caused when bacteria stick
to the walls of the bladder, kidney or the
opening of the urethra and then multiply.

Urobilinogen NEGATIVE 0 – 8mg/dl NORMAL

Increased values
 overburdening of the liver
 excessive RBC breakdown
 increased urobilinogen production
 re-absorption - a large hematoma
 restricted liver function
 hepatic infection
 poisoning
 liver cirrhosis

Low values
 failure of bile production
 obstruction of bile passage
 Blood NEGATIVE Negative NORMAL

Blood in the urine is a common problem.

The medical term for red blood cells in the
urine is hematuria. Sometimes blood in the
urine is a sign of a serious problem in the
urinary tract, while other times it is not
serious and requires no treatment. Only
after a thorough evaluation by a health-
care provider should blood in the urine be
attributed to a nonserious cause.

Ketone NEGATIVE Negative NORMAL

A negative test result is normal. When

ketones are present in the urine, the
results are usually listed as small,
moderate, or large with these
corresponding values:
Small: < 20 mg/dL
Moderate: 30 - 40 mg/dL
Large: > 80 mg/dL

Bilirubin NEGATIVE Negative NORMAL

It is breakdown product of hemoglobin.

Most of the bilirubin produced in humans is
conjugated by the liver and excreted into
the bile, but a very small amount of
conjugated bilirubin is reabsorbed and
reaches the general circulation to be
excreted in the urine. The normal level of
urinary bilirubin is below the detection limit
of the test. Bilirubin in the urine is derived
from the liver, and a positive test indicates
hepatic disease or hepatobiliary
obstruction.

SERUM
 TEST RESULT REFERENCE INTERPRETATION
VALUES

Creatinine 4.0 0.70 – 1.20 mg/dl INCREASED

 Increase in serum creatinine is seen any

renal functional impairment. Because of
its insensitivity in detecting early renal
failure, the creatinine clearance is
significantly reduced before any rise in
serum creatinine occurs. The renal
impairment may be due to intrinsic renal
lesions, decreased perfusion of the
kidney, or obstruction of the lower
urinary tract.

 A decreased creatinine clearance rate

may also occur when there is decreased
blood flow to the kidneys as may occur
with congestive heart failure, obstruction
within the kidney, or acute or chronic
kidney failure. The less effective the
kidney filtration, the greater the
decrease in clearance.

Sodium 138.0 137.00 – 145.00 NORMAL

mmol/L
 Increase in serum sodium is seen in
conditions with water loss in excess of
salt loss, as in profuse sweating, severe
diarrhea or vomiting, polyuria (as in
diabetes mellitus or insipidus),
hypergluco- or mineralocorticoidism, and
inadequate water intake. Drugs causing
elevated sodium include steroids with
mineralocorticoid activity,
carbenoxolone, diazoxide, guanethidine,
licorice, methyldopa, oxyphenbutazone,
sodium bicarbonate, methoxyflurane,
and reserpine.

 Decrease in sodium is seen in states

characterized by intake of free water or
hypotonic solutions, as may occur in fluid
replacement following sweating,
 diarrhea, vomiting, and diuretic abuse.
Dilutional hyponatremia may occur in
cardiac failure, liver failure, nephrotic
syndrome, malnutrition, and SIADH.
There are many other causes of
hyponatremia, mostly related to
corticosteroid metabolic defects or renal
tubular abnormalities. Drugs other than
diuretics may cause hyponatremia,
including ammonium chloride,
chlorpropamide, heparin,
aminoglutethimide, vasopressin,
cyclophosphamide, and vincristine.

Potassium 5.9 3.50 – 5.10 NORMAL

mEq/L
 Increase in serum potassium is seen in
states characterized by excess
destruction of cells, with redistribution of
K+ from the intra- to the extracellular
compartment, as in massive hemolysis,
crush injuries, hyperkinetic activity, and
malignant hyperpyrexia. Decreased renal
K+ excretion is seen in acute renal
failure, some cases of chronic renal
failure, Addison's disease, and other
sodium-depleted states. Hyperkalemia
due to pure excess of K+ intake is usually
iatrogenic.


 Decrease in serum potassium is seen

usually in states characterized by excess
K+ loss, such as in vomiting, diarrhea,
villous adenoma of the colorectum,
certain renal tubular defects,
hypercorticoidism, etc. Redistribution
hypokalemia is seen in glucose/insulin
therapy, alkalosis (where serum K+ is lost
into cells and into urine), and familial
periodic paralysis. Drugs causing
hypokalemia include amphotericin,
carbenicillin, carbenoxolone,
corticosteroids, diuretics, licorice,
salicylates, and ticarcillin.
 COAGULATION PROFILE

PROTHROMB RESULT REFERENCE INTERPRETATION

IN TIME VALUES

Patient 10.4 9 – 13 sec NORMAL

A prolonged, or increased, PT means that

your blood is taking too long to form a clot.
This may be caused by conditions such as
liver disease, vitamin K deficiency or a
coagulation factor deficiency. Result of the
PT is often interpreted with that of the PTT
in determining what condition may be
present.

Control 10.6 10.3 – 13.1 sec NORMAL

Activities 115.7 70 – 120 % NORMAL

INR 0.98 = / < 1.2 NORMAL

PARTIAL RESULT REFERENCE INTERPRETATION

THROMBOPLA VALUES
STIN TIME

Patient 29.3 30 – 43 SEC NORMAL

A longer-than-normal PTT or APTT can be

caused by liver disease, kidney disease
(such as nephrotic syndrome), or
treatment with blood thinners, such as
heparin or warfarin (Coumadin).

Control 36.4 30 – 38.2 SEC NORMAL

COMPLETE BLOOD COUNT

 TEST RESULT REFERENCE INTERPRETATION
VALUES

WBC 7.44 5 - 11 NORMAL

White blood cells are bigger than red blood

cells but fewer in number. When a person
has a bacterial infection, the number of
white cells rises very quickly. The number
of white blood cells is sometimes used to
find an infection or to see how the body is
dealing with cancer treatment.

RBC 3.06 F: 4.2 – 5.4 ABNORMAL

If the RBC count is low (anemia), the body

may not be getting the oxygen it needs. If
the count is too high (a condition called
polycythemia), there is a chance that the
red blood cells will clump together and
block tiny blood vessels (capillaries). This
also makes it hard for your red blood cells
to carry oxygen.

Hemoglobin 9.5 F: 12.0 – 16.0 ABNORMAL

Low hemoglobin levels are usually due to

nutritional deficiency especially iron
deficiency. If you are not consuming the
required daily amount of iron, vitamin B12
and folate, you are going to have the
problem of low hemoglobin levels. One of
the reasons for perpetually low hemoglobin
levels is a bone marrow problem. Among
temporary reasons of low hemoglobin
levels we have accidents or surgeries that
led to severe loss of blood and medications
that may affect hemoglobin levels.

Hematocrit 28.6 F: 38 - 47 ABNORMAL

Low hematocrit may be due to:

 Anemia
 Bleeding
 Destruction of red blood cells
  Leukemia
 Malnutrition
 Nutritional deficiencies of iron, folate,
vitamin B12, and vitamin B6
 Overhydration

MCV 93.5 80 – 100 fL NORMAL

(Mean cell
Volume)

MCH 31.0 27 – 33 NORMAL

(Mean Cell
Hemoglobin) It measures the amount of hemoglobin
present in one RBC. The weight of
hemoglobin in an average cell is obtained
by dividing the hemoglobin by the total
RBC count. The result is reported by a very
small weight called a picogram (pg).

MCHC 33.2 31 - 36 NORMAL

(mean
corpuscular It measures the proportion of each cell
hemoglobin taken up by hemoglobin. The results are
concentration) reported in percentages, reflecting the
proportion of hemoglobin in the RBC. The
hemoglobin is divided by the hematocrit
and multiplied by 100 to obtain the MCHC.

RDW – CV NORMAL
(red blood cell 13.7 11 - 16
distribution –
coefficient
variation)

RDW – SD 46.6 37 - 54 NORMAL

(red blood cell
distribution-
standard
deviation)

PLATELET 259.0 150 - 400 NORMAL

A normal platelet count ranges between

 150,000 and 450,000. Thrombocytopenia
occurs when the platelet count drops below
50,000. A thrombocytopenic patient is at
high risk for bleeding if he or she has an
injury or a complicating condition that
affects blood coagulation, such as
hemophilia or liver disease. When the
platelet count drops below 20,000, the
patient may have spontaneous bleeding
that may result in death. A report of
"adequate platelets" implies that there is
at least one platelet for every 20 red blood
cells.
DIFFERENTIA
L COUNT

Neutrophil 0.68 0.55 – 0.77 NORMAL

In addition to bacterial infections,

neutrophil counts are increased in many
inflammatory processes, during physical
stress, or with tissue necrosis that might
occur after a severe burn or a myocardial
infarction. Neutrophils are also increased in
granulocytic leukemia.

A decrease in neutrophils is known as

neutropenia

Lymphocyte 0.19 0.27 – 0.33 ABNORMAL

Lymphocytes are made in the bone
marrow which means that when the bone
marrow isn’t functioning properly,
lymphocyte counts can drop. This can
occur in a condition known as aplastic
anemia. There are also certain inherited
conditions where the body doesn’t make
enough immune cells, resulting in a
decrease in lymphocytes.

Monocyte 0.09 0 – 0.12 NORMAL

Eosinophils 0.04 0 – 0.07 NORMAL

Basohphils 0.00 0 .01 – 0.05 ABNORMAL

Basophils are non-phagocytic cells which,

when activated, release numerous
compounds from the basophilic granules
within their cytoplasm. They play a major
role in allergic responses, particularly type
I hypersensitive reactions.
DRUG STUDY
GENERIC
NAME / CLASSIFICA MECHANIS INDICATION CONTRAINDIC SIDE EFFECT / NURSING
BRAND TION M ATION ADVERSE RESPONSIBILITIES
NAME OF REACTION
ACTION
 Insulin  Monitor for fasting
Insulin Anti – Decrese Management Hypoglycemia; resistance blood glucose, 2
(Humulin diabetic blood of type 1 DM insulinoma;  Allergic hours after meals
70/30) drugs glucose; by and type 2 hypersensitivit reactions (80-150mg/dl,
transport DM. y reactions  Edema normal fasting
of glucose  Refraction level; 70-
32 units into cells anomalies 130mg/dl, normal
– 0 – 28 and the 2-hr level)
 lipodystroph
units conversion  Monitor body
y
of glucose weight
to periodically;
glycogen changes in weight
indirectly may necessitate
increases changes in insulin
blood dose
pyruvate  Assess for
and hypoglycemia/hyp
lactate, erglycemia
decrease  Instruct patient on
phosphate proper technique
and for administration.
potassium.

Allopurin Analgesics, Inhibits Treatment of Severe renal  Drowsiness  Assess for pain
ol Muscle xanthine primary or impairment  Renal failure including location,
(Llanol) relaxants oxidase, an secondary and children  uremia characteristics,
 and enzyme gout, except those  alopecia onset/duration,
100mg/t Uricosurics involved in hyperuricemi with  nausea/vomi frequency, quality,
ab the a resulting hyperuricemia ting intensity/severity,
synthesis from secondary to  diarrhea precipitating
of uric acid chemotherap malignancy,  fever factors
without hy for idiopathic  Monitor uric acid
 leucopenia
disrupting malignancies, hemochromat levels every 2
 anemia
the recurrent osis, acute weeks (normal:
biosynthesi calcium gouty attack;  hepatitis
<6mg/dl)
s of oxalate renal hypersensitivit  Monitor renal
essential calculi. y; lactation function
purine. Recurrent  Advise patient to
Results in tophaceous avoid caffeine and
decreased deposits or alcohol for these
uric acid uric acid may increase uric
level. stones acid levels

 Allergic  Accidental
Iberet Vitamins Iron is Treatment & Thalassemia, reactions overdose of iron-
needed to prevention of sideroblastic  GI effects containing
500mg produce Fe-deficiency anemia,  Hyperbilirubi products can be
hemoglobi & hemochromat nemi very dangerous
n (Hb). In concomitant osis &  bright yellow and even fatal.
the case of folic acid hemosiderosis urine  Do not start or
iron deficiency w/ . discoloration stop any medicine
deficiency, associated without doctor or
 flushing
smaller red deficient pharmacist
 dizziness or
blood cell intake or approval.
faintness
with lower increased  Take the missed
Hb content need for vit  peripheral
sensory dose as soon as
is formed, B-complex in you remember; do
which may nonpregnant neuropathie
s not take if it is
 lead to adults.  stone almost time for
hypochrom formation, the next dose.
ic crystalluria Instead, skip the
microcytic & oxalosis missed dose and
anemia.  black resume your usual
Vitamin C discoloration dosing schedule.
helps body of stool. Do not "double-
metabolis up" the dose to
m. Vitamin catch up
B-complex
plays an
important
role as co-
enzyme in
protein
metabolis
m. Folic
Acid:
Deficiency
in folic acid
as well as
in vitamin
B12 will
affect
hematopoi
esis.

Rosuvast Dyslipidae It produces  Adjunct to Active liver  headac  Prior to therapy,

atin mic Agents its lipid- diet to disease or w/ he assess patient for
(Crestor) modifying reduce unexplained  myalgia underlying causes
effects in elevated persistent  astheni of
10mg/ta two ways. total-C, elevations of a hypercholesterole
b First, it LDL-C, serum  constip mia
increases ApoB, transaminases ation  Monitor total
the nonHDL-C . Pregnancy &  dizzines cholesterol, LDL
number of & TG levels lactation. s and HDL
hepatic & to  nausea  Instruct patient to
LDL increase  abdomi take drug exactly
receptors HDL-C in nal pain as prescribed.
on the cell- patients w/  Follow cholesterol-
 priritus
surface to primary lowering diet and
 rash
enhance hyperlipide exercise regimen
uptake and mia &  hyperse
nsitivity as prescribed.
catabolism mixed  Avoid alcohol.
of LDL. dyslipidemi reactions
Second, a. Adjunct
rosuvastati to diet in
n inhibits patients w/
hepatic hyperglyce
synthesis ridemia
of VLDL,  Patients w/
which homozygou
reduces s familial
the total hyperchole
number of ste-rolemia
VLDL and to reduce
LDL LDL-C,
particles. total-C and
ApoB.
Adjunct to
diet in
slowing
atheroscler
osis
 progression
as part of
treatment
strategy to
lower total-
C and LDL-
C.

Bumetan Loop Increases Hypertension Anuria;  Electrolyte  Monitor for

ide diuretics excretion ; edema hepatic coma; imbalance in manifestations of
(Burinex) of water, associated severe prolonged hypokalemia;
sodium with electrolyte treatment hypocalcemia;
and congestive depletion  Muscular hypomagnesemia;
1 mg/tab potassium, heart failure; cramps hyponatremia and
calcium hepatic renal  Skin rashes hyperchloremia
and disease  Monitor
chloride; including electrolytes
decreases nephritic  If GI symptoms
uric acid syndrome occur, instruct the
secretion and acute patient to take
and cause pulmonary with food or milk
no change edema  Instruct the
in urinary patient to contact
pH. physician
immediately if
irregular heart
beat or fluttering
of chest,
abdominal pain,
hearing loss,
muscle cramps,
weakness, nausea,
 dizziness or
numbness occur.

Sulodexi Anticoagul It is used Vascular Hypersensitivi For Capsule:  Assess patient

de ants, as pathologies ty to  Nausea/vo physical and
(Vessel Antiplatelet hypolipoda w/ thrombotic sulodexide, miting laboratory
Due-F) s& emic and risk, transient heparin &  Epigastralgi examination
Fibrinolytic anti- ischemic heparin-like a  Evaluate patient
250 s thrombotic attacks & products. For Ampule: allergic reaction
(Thromboly . cerebrovascu Diathesis &  Pain  Monitor patient BP
tics) lar disease, hemorrhagic  Burn and heart rate
peripheral diseases.  Teach patient to
 Hematoma
vascular report and monitor
at injection
insufficiency, any adverse
site
diabetic reaction during
retinopathy, therapy
MI, retinal
vasal
thrombosis.

Gabapen CNS Mechanism Adjunctive Hypersensitivi  Hypertensio  Assess mental

tin depressant unkown. therapy: ty to drug. n status and report
(Neuront s Prevents partial  Somnolenc abnormalities.
in) and treats seizures with e  Assess patient’s
partial and without  Dizziness disorder before
600mg/t seizures secondary  Ataxia starting therapy.
ab and generalizatio  Monitor for
 Tremor
postherpeti n in adults possible drug
 Nervousnes
c with epilepsy. induced adverse
s
neuralgia. Neuropathic reaction.
Structurall pain, diabetic  Amnesia
y similar to neuropathy,  Depression
 GABA but post-herpetic
does not and
interact trigeminal
with GABA neuralgia.
receptors.

Warfarin Anticoagul Inhibits Prophylaxis Pregnancy;  Hemorrhag  Assess patient’s

(Coumad ant; vitamin K and/or blood e condition before
in) prophylaxis dependent treatment dyscrasias,  Necrosis therapy and
activation thrombosis, bleeding  Alopecia regularly to
2.5mg of clotting pulmonary tendicies  Urticaria monitor drug
factors II, embolism, associated effectiveness.
 Fever
VII, IX and atrial with active  Monitor for
 Diatthea
X formed fibrillation ulceration. possible drug
in the liver. with  GI
induced adverse
It reduces embolization, disturbance
reaction.
the ability adjunct in s
 Regularly assess
of blood to prophylaxis for bleeding.
clot. of systemic  Monitor
embolism coagulation
after MI. parameters.

DRUG CLASSIFICA DOSAGE INDICATION CONTRA ADVERS NURSING

TION INDICATION REACTION CONSIDERATION
ARIXTRA Thromboliti 2.5mg Prevention of Clinically Anemia,
cs venous significant bleeding,
thromboemb bleeding, purpura,
olic events in acute edema
patient bacterial
undergoing endocarditis.
major
 orthopedic
surgery of
the lower
limbs.
Treatment of
acute DVT,
pulmonary
embolism,
unstable
angina or
non-ST
segment
elevation MI,
acute
coronary
syndrome for
the
FIBROSI 1 sachet prevention of >may be mixed with
NE Laxatives daily death. Of food or beverage
bowel
movement

Fiber
supplement
to maintain
regularity

SENOKO Hepatic 2 tabs Acute surgical Mild

T Protector abdomen, abdominal
abdominal discomfort,
 pain, nausea, diarrhea with
Functional vomiting or excessive loss
constipation symptoms of of water and
of appendicitis: electrolytes,
hospitalized intestinal atonic non
patient, O hemorrhage, functional
and G persistent colon
patient, post diarrhea
surgical
prenatal,
postpartum,
geriatric
patient,
APPETITE 1 sachet functional
KALIMAT ENHANCER daily constipation Patient’s with
E due to intake intestinal Constipation,
of certain obstruction anorexia and
drugs and stenosis, nausea
constipation

Prevention
and
treatment of
hyperkalemia
resulting
fromacute or
chronic renal
failure
 NURSING CARE PLAN
CUES NURSING GOALS AND INTERVE RATIONALE EVALUATI
DIAGNOSI OBEJECTIVE NTIONS ON
S S
Subjective: Acute pain After 8 hours After
related to of nursing nursing
• The client edema intervention interventio
complains formation the n, the
of feeling as Patient’s pain patient’s
of evidenced will be pain is
numbness by verbal lessened. lessened.
in her both reports.
feet, when
asked if the
client feels Objectives:
pain, the Independ Only the client
client ent: can judge the
verbalized 1. The Encourage level and
“masakit patient will patient to distress of pain;
ang paa ko be able to verbalize pain
pag verbalize the about management
nagagalaw, characteristic pain. should be a
o kaya ay and location team approach
napipisil, of pain. that includes
lalo na pag the client. Very
naglalakad few people lie
ako.” about pain.

Provide
• The client comfort
rate her 2. The measures Deep breathing
pain 6/10 patient will such as for relaxation is
as 10 being be able to deep easy
the highest perform pain breathing to learn and
and 1 management exercises contributes to
being the . like pain relief and
lowest. meditation reduction by
. reducing
muscle tension
Objectives: and anxiety.
Provide
• When both therapeuti The human
feet are c touch. body is
palpated believed to
with light have energy
 pressure fields that
added express
facial aberrant
grimace patterns when
were body systems
noted. are
insulted.
Therapeutic
BP: 130/90 Touch is
RR: 20cpm Advice thought to
PR: 82bpm 3. The patient to realign
patient will take rest aberrant fields.
be able to periods.
perform
chosen Encourage
diversional diversional To prevent
activities. activities fatigue
(TV/radio,
socializati
on with
others,ima
gery) To divert
attention from
pain.

Collabora
tive:
Administer
3. On the analgesics
given time, as ordered
pain reliever
is
administered
to the Necessary for
patient. Monitor treatment of
patient’s the
vital signs. underlying
cause.
An analgesic is
4. After any member of
every 4 the group
hours, the of drugs used
patient’s to relieve pain
vital
 signs will be
monitored.

MANAGEMENT AND TREATMENT FOR DVT

• Anticoagulation
is the usual treatment for DVT. In general, patients are initiated on a
brief course (i.e., less than a week) of heparin treatment while they start on
a 3- to 6-month course of warfarin(or related vitamin K inhibitors)

• Thrombolysis
is generally reserved for extensive clot, e.g. an iliofemoral thrombosis.
In July 2008, the American College of Chest Physicians (ACCP) published new
evidence-based clinical guidelines for the treatment of venous
thromboembolic (VTE) disease which for the first time suggested the use of
pharmacomechanical thrombolysis in the treatment of certain cases of acute
DVT.

• Thrombectomy
Thrombus can be removed with a mechanical thrombectomy device.
Combination therapy that uses mechanical thrombectomy to deliver
localized thrombolytics has recently received considerable attention as a
treatment for DVT.

• Compression stockings
Elastic compression stockings should be routinely applied "beginning
within 1 month of diagnosis of proximal DVT and continuing for a minimum
of 1 year after diagnosis". Starting within one week may be more effective.
They reduce the risk of postthrombotic syndrome. The stockings in almost all
trials were stronger than routine anti-embolism stockings and created either
20–30 mm Hg or 30–40 mm Hg. Most trials used knee-high stockings.

• Inferior vena cava filter

reduces pulmonary embolism[ and is an option for patients with an
absolute contraindiciation to anticoagulant treatment (e.g., cerebral
hemorrhage) or those rare patients who have objectively documented
recurrent PEs while on anticoagulation, an inferior vena cava filter (also
referred to as a Greenfield filter) may prevent pulmonary embolisation of the
leg clot. However these filters are themselves potential of thrombosis, IVC
filters are viewed as a temporizing measure for preventing life-threatening
pulmonary embolism.

• Hospitalization
Treatment at home is an option according to a meta-analysis by the
Cochrane Collaboration. Hospitalization should be considered in patients with
more than two of the following risk factors as these patients may have more
risk of complications during treatment:
• bilateral DVT
• renal insufficiency
• low body weight (<70 kg/154 lbs)
• recent immobility
• chronic heart failure
• cancer
Diabetes Treatment
(Treatment of Diabetes Mellitus)

• Monitoring blood sugar

If you've just received a diagnosis of diabetes, monitoring your blood

sugar may seem like an overwhelming task. But once you learn to
measure your blood sugar and understand how important it is, you'll
feel more comfortable with the procedure and more in control of your
disease. Testing is crucial because it tells you whether you're keeping
your glucose levels in the range you and your doctor have agreed on.

The best range for you depends on your age and the type of diabetes
you have. For younger adults who don't have complications of
diabetes, a typical target range might be 80 to 120 mg/dL before
meals, and below 180 mg/dL after eating. Older adults who have
complications from their disease may have a fasting target goal of 100
to 140 mg/dL and below 200 mg/dL after meals. That's because blood
sugar that falls too low in older adults can be more dangerous than in
younger people.

How often you test your blood sugar depends on the type of diabetes
you have. If you take insulin, test your blood sugar at least twice a day,
and preferably three or four times a day. But if you have type 2
diabetes and don't use insulin, you may need to test your blood sugar
levels only once a day or as little as twice a week.

Keep in mind that the amount of sugar in your blood is constantly

changing. Self-monitoring helps you learn what makes your blood
sugar levels rise and fall, so you can make adjustments in your
treatment. Factors that affect your blood sugar include:
• Food. Food raises your blood sugar level ? it's highest one to two
hours after a meal. What and how much you eat, and the time of day,
also affect your blood sugar level.

• Exercise and physical activity. In general, the more active you are,
the lower your blood sugar. Physical activity causes sugar to be
transported to your cells, where it's used for energy, thereby lowering
the levels in your blood. Aerobic exercises such as brisk walking,
jogging or biking are especially good. But gardening, housework and
even just being on your feet all day also can lower your blood sugar.

• Medications. Insulin and oral diabetes medications deliberately work

to lower your blood sugar. But medications you take for other
conditions may affect glucose levels. Corticosteroids, in particular, may
raise blood sugar levels. Medications such as thiazides, used to control
high blood pressure, and niacin, used for high cholesterol, also may
increase blood sugar. If you need to take certain high blood pressure
medications, your doctor will likely make changes in your diabetes
treatment.

• Illness. The physical stress of a cold or other illness causes your body
to produce hormones that raise your blood sugar level. The additional
sugar helps promote healing. But if you have diabetes, this can be a
problem. In addition, a fever increases your metabolism and how
quickly sugar is utilized, which can alter the amount of insulin you
need. For these reasons, be sure to monitor your glucose levels
frequently when you're sick.

• Alcohol. Even a small amount of alcohol ? about 2 ounces ? can cause

your sugar levels to fall too low. But sometimes alcohol can cause
sugar levels to rise. If you choose to drink, do so only in moderation.
And monitor your blood sugar before and after consuming alcohol to
see how it affects you. Also, keep in mind that alcohol counts as
carbohydrate calories in your diet.

• Fluctuations in hormone levels. The female hormone estrogen typically

makes cells more responsive to insulin, and progesterone makes cells
more resistant. Although these two hormones fluctuate throughout the
menstrual cycle, the majority of women don't notice a corresponding
change in blood sugar levels. Those who do are more likely to
experience changes in blood sugar during the third week of their
menstrual cycle, when estrogen and progesterone levels are highest.
 • Hormone levels also fluctuate during perimenopause ? the time before
menopause. How this affects blood sugar varies, but most women can
control any symptoms with additional exercise and changes in their
diet. If your symptoms are more severe, your doctor may recommend
oral contraceptives or hormone replacement therapy (HRT). After
menopause, many women with diabetes require about 20 percent less
medication because their cells are more sensitive to insulin.

A healthy diet

• Contrary to popular myth, there's no "diabetes diet." Furthermore,

having diabetes doesn't mean you have to eat only bland, boring
foods. Instead, it means you'll eat more fruits, vegetables and whole
grains ? foods that are high in nutrition and low in fat and calories ?
and fewer animal products and sweets. Actually, it's the same eating
plan all Americans should follow.

• Yet understanding what and how much to eat can be a challenging

task. Fortunately, a registered dietitian can help you put together a
meal plan that fits your health goals, food preferences and lifestyle.
Once you've decided on a meal plan, keep in mind that consistency is
extremely important. To keep your blood sugar at a consistent level,
try to eat the same amount of food with the same proportion of
carbohydrates, proteins and fats at the same time every day.

• But even with all the information you need and the best intentions,
sticking to your diet can be one of the most challenging parts of living
with diabetes. The key is to find ways to stay motivated. Don't let
others undermine your determination to eat in the healthiest way
possible. You have to believe that what you're doing matters ? and that
you're worth it.

• Exercise
Everyone needs regular aerobic exercise, and people with diabetes are
no exception. The good news is that the same exercises that are good
for your heart and lungs also help lower your blood sugar levels.

See your doctor before beginning any exercise program. Once you
have the go-ahead, take some time to think about which activities you
enjoy and are likely to stick with. Walking, hiking, jogging, biking,
tennis, cross-country skiing and swimming are all good choices.

Aim for at least 30 minutes of aerobic exercise most days. But if you
haven't been active for a while, start slowly and build up gradually. For
 the best results, combine your aerobic activity with stretching and
strength-training exercises.

• Healthy weight

Being overweight is the greatest risk factor for type 2 diabetes. That's
because fat makes your cells more resistant to insulin. But when you
lose weight, the process reverses and your cells become more
receptive to insulin. For some people with type 2 diabetes, weight loss
is all that's needed to restore blood sugar to normal. Furthermore, a
modest weight loss of 10 to 20 pounds is often enough.

Yet losing even 10 pounds can be a challenge for most people.

Fortunately, you don't have to do it alone. A registered dietitian can
help you develop a weight-loss plan that takes into account your
current weight, activity level, age and overall health. Ultimately,
however, the motivation has to come from you.

• Medications

When diet, exercise and maintaining a healthy weight aren't enough,

you may need the help of medication. Medications used to treat
diabetes include insulin. Everyone with type 1 diabetes and some
people with type 2 diabetes must take insulin every day to replace
what their pancreas is unable to produce. Unfortunately, insulin can't
be taken in pill form because enzymes in your stomach break it down
so that it becomes ineffective. For that reason, many people inject
themselves with insulin using a syringe or an insulin pen injector ? a
device that looks like a pen, except the cartridge is filled with insulin.
Others may use an insulin pump, which provides a continuous supply
of insulin, eliminating the need for daily shots.

An insulin pump is a pumping device about the size of a deck of cards.

You wear it outside your body. A small tube connects the reservoir of
insulin to a catheter that's inserted under the skin of your abdomen.
The pump dispenses the desired amount of insulin into your body and
can be adjusted to infuse more or less insulin depending on meals,
activity and glucose level. Insulin pumps aren't for everyone. But for
some people they provide improved blood sugar control and a more
flexible lifestyle.

The most widely used form of insulin is synthetic human insulin, which
is chemically identical to human insulin but manufactured in a
laboratory. Unfortunately, synthetic human insulin isn't perfect. One of
its chief failings is that it doesn't mimic the way natural insulin is
secreted. But newer types of insulin, known as insulin analogs, more
closely resemble the way natural insulin acts in your body. Among
these are lispro (Humalog), insulin aspart (NovoLog) and glargine
(Lantus).

A number of drug options exist for treating type 2 diabetes, including:

Sulfonylurea drugs. These medications stimulate your pancreas to

produce and release more insulin. For them to be effective, your
pancreas must produce some insulin on its own. Second-generation
sulfonylureas such as glipizide (Glucotrol, Glucotrol XL), glyburide
(DiaBeta, Glynase PresTab, Micronase) and glimepiride (Amaryl) are
prescribed most often. The most common side effect of sulfonylureas
is low blood sugar, especially during the first four months of therapy.
You're at much greater risk of low blood sugar if you have impaired
liver or kidney function.

Meglitinides. These medications, such as repaglinide (Prandin), have

effects similar to sulfonylureas, but you're not as likely to develop low
blood sugar. Meglitinides work quickly, and the results fade rapidly.

Biguanides. Metformin (Glucophage, Glucophage XR) is the only drug

in this class available in the United States. It works by inhibiting the
production and release of glucose from your liver, which means you
need less insulin to transport blood sugar into your cells. One
advantage of metformin is that is tends to cause less weight gain than
do other diabetes medications. Possible side effects include a metallic
taste in your mouth, loss of appetite, nausea or vomiting, abdominal
bloating, or pain, gas and diarrhea. These effects usually decrease over
time and are less likely to occur if you take the medication with food. A
rare but serious side effect is lactic acidosis, which results when lactic
acid builds up in your body. Symptoms include tiredness, weakness,
muscle aches, dizziness and drowsiness. Lactic acidosis is especially
likely to occur if you mix this medication with alcohol or have impaired
kidney function.

Alpha-glucosidase inhibitors. These drugs block the action of

enzymes in your digestive tract that break down carbohydrates. That
means sugar is absorbed into your bloodstream more slowly, which
helps prevent the rapid rise in blood sugar that usually occurs right
after a meal. Drugs in this class include acarbose (Precose) and miglitol
(Glyset). Although safe and effective, alpha-glucosidase inhibitors can
cause abdominal bloating, gas and diarrhea. If taken in high doses,
they may also cause reversible liver damage.
 Thiazolidinediones. These drugs make your body tissues more
sensitive to insulin and keep your liver from overproducing glucose.
Side effects of thiazolidinediones, such as rosiglitazone (Avandia) and
pioglitazone hydrochloride (Actos), include swelling, weight gain and
fatigue. A far more serious potential side effect is liver damage. The
thiazolidinedione troglitzeone (Rezulin) was taken off the market in
March 2000 because it caused liver failure. If your doctor prescribes
these drugs, it's important to have your liver checked every two
months during the first year of therapy. Contact your doctor
immediately if you experience any of the signs and symptoms of liver
damage, such as nausea and vomiting, abdominal pain, loss of
appetite, dark urine, or yellowing of your skin and the whites of your
eyes (jaundice). These may not always be related to diabetes
medications, but your doctor will need to investigate all possible
causes.

Drug combinations. By combining drugs from different classes, you

may be able to control your blood sugar in several different ways. Each
class of oral medication can be combined with drugs from any other
class. Most doctors prescribe two drugs in combination, although
sometimes three drugs may be prescribed. Newer medications, such
as Glucovance, which contains both glyburide and metformin, combine
different oral drugs in a single tablet.

• Transplantation

In recent years, researchers have focused increasing attention on

transplantation for people with type 1 diabetes. Current procedures
include:

Pancreas transplantation. Pancreas transplants have been

performed since the late 1960s. Most are done in conjunction with or
after a kidney transplant. Kidney failure is one of the most common
complications of diabetes, and receiving a new pancreas when you
receive a new kidney may actually improve kidney survival.
Furthermore, after a successful pancreas transplant, many people with
diabetes no longer need to use insulin. Unfortunately, pancreas
transplants aren't always successful. Your body may reject the new
organ days or even years after the transplant, which means you'll need
to take immunosuppressive drugs the rest of your life. These drugs are
costly and can have serious side effects, including a high risk of
infection and organ injury. Because the side effects can be more
dangerous to your health than your diabetes, you're usually not
considered a candidate for transplantation unless your diabetes can't
be controlled or you're experiencing serious complications. On the
 other hand, pancreas transplantation may be an option if you are age
45 or younger, have type 1 diabetes and need or have had a kidney
transplant, or if insulin doesn't control your blood sugar.

Islet cell transplantation. Your pancreas contains about 1 million

islet cells, 75 percent to 80 percent of which produce insulin. The beta
cells that produce insulin reside in the islets. Although still considered
an experimental procedure, transplanting these cells may offer a less
invasive, less expensive and less risky option than a pancreas
transplant for people with diabetes. In islet cell transplantation, doctors
infuse fresh pancreas cells into the liver of the person with diabetes.
The cells spread throughout the liver and soon begin to produce
insulin. The liver, not the pancreas, is the site of the transplant
because it's easier to access the large portal vein in your liver than it is
to access a vein in your pancreas. What's more, cells that grow in the
liver secrete insulin much like cells in the pancreas do.

Alternative Treatment For Diabetes

Alternative Therapies for Diabetes

Alternative therapies are treatments that are neither widely taught in

medical schools nor widely practiced in hospitals. Alternative treatments that
have been studied to manage diabetes include acupuncture, biofeedback,
guided imagery, and vitamin and mineral supplementation. The success of
some alternative treatments can be hard to measure.

• Acupuncture

Acupuncture is a procedure in that a practitioner inserts needles into

designated points on the skin. Some Western scientists believe that
acupuncture triggers the release of the body's natural painkillers.
Acupuncture has been shown to offer relief from chronic pain.
Acupuncture is sometimes used by people with neuropathy, the painful
nerve damage of diabetes.

• Biofeedback

Biofeedback is a technique that helps a person become more aware of

and learn to deal with the body's response to pain. This alternative
therapy emphasizes relaxation and stress-reduction techniques.
Guided imagery is a relaxation technique that some professionals who
use biofeedback do. With guided imagery, a person thinks of peaceful
mental images, such as ocean waves. A person may also include the
images of controlling or curing a chronic disease, such as diabetes.
 People using this technique believe their condition can be eased with
these positive images.

• Chromium

The benefit of added chromium for diabetes has been studied and
debated for several years. Several studies report that chromium
supplementation may improve diabetes control. Chromium is needed
to make glucose tolerance factor, which helps insulin improve its
action. Because of insufficient information on the use of chromium to
treat diabetes, no recommendations for supplementation yet exist.

• Magnesium

Although the relationship between magnesium and diabetes has been

studied for decades, it is not yet fully understood. Studies suggest that
a deficiency in magnesium may worsen the blood sugar control in type
2 diabetes. Scientists believe that a deficiency of magnesium
interrupts insulin secretion in the pancreas and increases insulin
resistance in the body's tissues. Evidence suggests that a deficiency of
magnesium may contribute to certain diabetes complications.

• Vanadium

Vanadium is a compound found in tiny amounts in plants and animals.

Early studies showed that vanadium normalized blood glucose levels in
animals with type 1 and type 2 diabetes. A recent study found that
when people with diabetes were given vanadium, they developed a
modest increase in insulin sensitivity and were able to decrease their
insulin requirements. Currently researchers want to understand how
vanadium works in the body, discover potential side effects, and
establish safe dosages.
DISCHARGE PLANNING

MEDICATIONS: Advise client to not discontinue taking medications

prescribed by her physician. This medications may include, Arixtra to prevent
recurrent or ongoing thrombolytic occlusion another medications are
Allopurinol, Vitamin B complex, Iberet, Rosuvastatin and Irbesartan.

EXERCISE: According to Investigators Against Thrombo Embolism (INATE),

recovery time is significantly reduced in patients who begin exercise
immediately after starting treatment. They recommend early, slow walking
exercises 24 hours after treatment followed by average daily walking
distances of 600 to 12,000 meters. Each patient is different and a physician
should be consulted about post DVT exercise on a case-by-case basis.
The American Council on Exercise suggests several simple exercises
travelers can do in their seats to prevent the development of DVT. These
exercises include: ankle turns, foot lifts, knee lifts, arm bends, shoulder rolls,
knee to chest lifts, forward bends, upper body stretches, shoulder stretches
and neck rolls.

TREATMENT:
Treatment for DVT includes:

• Hospitalization
• Intravenous drugs to dissolve the clot
• Long term treatment with anticoagulant drugs, such as Warfarin, to
prevent further clotting
• Blood tests to monitor the 'stickiness' of the blood
• Reducing risk factors such as losing excess body fat and switching to a
low fat diet.

HEALTH TEACHING:
The ff. Health Teachings are directed towards the patient for the
betterment of her condition and also serves as chain of continuing health
promoted by Health Care Providers even after discharge.
• Advice client to comply with the medications that will be given by her
physician.
• Advice client to avoid dangling her feet. The feet should be elevated.
• Advice client to avoid skipping meals, eating something which is not
allowed or drinking to much.
 • Advice client to avoid massaging the affected part.
• Advice client to don't sit with the legs crossed.
• Advice client to drink plenty of fluids.

OUTPATIENT DEPARTMENT/ FOLLOW UP CHECK UP: Remind the patient with

an immediate family member for a follow-up appointment in the hospital 1-2
weeks after discharge or when complications of the disease appear or when
the physician said.

DIET: Her diet should be in a low fat diet, high fiber, and apparently orange
juice, natural remedies containing vitamin K on the off list too because it
may interact to the medications.

EVIDENCE-BASED NURSING

REVIEW: ELASTIC COMPRESSION STOCKINGS PREVENT POST-

THROMBOTIC SYNDROME IN PATIENTS WITH DEEP VENOUS
THROMBOSIS

Question: Are non-pharmaceutical interventions effective and safe

for preventing post-thrombotic syndrome (PTS) in patients with
deep venous thrombosis (DVT)?

METHODS

Data sources:

Cochrane Peripheral Vascular Diseases Specialised Trials Register

(January 2003), which is based on searches of Medline and EMBASE/Excerpta
Medica; Cochrane Central Register of Controlled Trials (2002); hand searches
of Scripta Phlebologica (1993–2000), J Thromb Haemost (2003), conference
proceedings, and citations of identified studies; and experts in the field.

Study selection and assessment:

Randomised controlled trials (RCTs) or clinical controlled trials that

compared medical elastic stockings (pressure 20–30 mm Hg or 30–40 mm Hg
at the ankle), compression bandages, or bed rest with control (no
intervention or placebo stockings) in patients with objectively diagnosed
DVT. Studies were assessed for validity and methods using a standard
checklist.
Outcomes:

Occurrence of PTS over time. Secondary outcomes included complications

and adverse effects (pulmonary embolism within 2 weeks of treatment,
discomfort, pain, swelling, pressure sores, and recurrence of thrombosis).

MAIN RESULTS

4 RCTs (n = 466) met the selection criteria; 3 (n = 421) were included in the
meta-analysis. At 2 years, patients who received elastic compression
stockings had greater reductions in the incidence of any or severe PTS than
those who received the control intervention (table). No information was
available for complications or adverse effects in these studies. In 1 RCT (n = 
45), patients who received a compression intervention had less pain and
swelling than those who received bed rest without compression for the first 9
days after DVT (p<0.05). Complications or adverse effects were similar
between the groups.

Elastic compression stockings v control (no intervention or placebo

stockings) for deep venous thrombosis*

CONCLUSIONS

Elastic compression stockings prevent post-thrombotic syndrome in patients

with deep venous thrombosis. Safety information was not available for the
pooled studies; 1 study found similar adverse effects between groups.

Commentary

Gloria Elton, RN, BScN

Estimates suggest that 1 in 3 patients with primary DVT will develop

PTS,1 which produces leg pain, swelling, and occasionally, leg ulceration.2
Previous research has shown that patients with PTS perceive that the disease
will have a negative impact on their quality of life.3 The review by Kolbach et
al suggests that elastic compression stockings significantly reduce the risk of
developing PTS. Earlier research indicates that although physicians
understand the role of compression stockings for reducing the incidence of
PTS, the impetus for ordering is the presence of symptoms, rather than
prevention.3

A potential weakness of the review by Kolbach et al is the unclear

description of initial and ongoing anticoagulant therapy. Subtherapeutic
anticoagulant therapy may be prognostic for the development of PTS, and
therefore it would be reassuring to confirm that anticoagulant therapy was
delivered similarly across trial arms to avoid confounding.4 Additionally, the
absence of a validated, universally approved, PTS scoring system can distort
the purported incidence. However, this is unlikely to bias the conclusions of
the review. The use of oversized stockings in 1 of the studies included in the
review (ie, Ginsberg et al) suggests that despite suboptimal compression,
compression stockings remain beneficial.

Further research is needed on the use of compression stockings in the

presence of arterial insufficiency. However, Kolbach et al provide a good
argument for the use of compression stockings as safe and effective for
prevention of PTS. Nurses should initiate their use before PTS symptoms
occur.