Case+Study Chronic Renal Failure
Case+Study Chronic Renal Failure
Case+Study Chronic Renal Failure
Failure
Nursingcasestudy.blogspot.com
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I. INTRODUCTION
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to control this complication of chronic kidney disease, improved patient outcomes
on in terms of morbidity and mortality will be achieved.
To ensure that the diagnosis of hyperparathyroidism is made early in the
course of chronic kidney disease, it is important to educate primary care
physicians, cardiologists, endocrinologists and other healthcare providers who
may see patients in the early stages of chronic kidney disease, so that they may
assess blood parathyroid hormone levels to uncover this complication and either
embark on the treatment of hyperparathyroidism or consider referral to a
nephrologist for further advice on the appropriate management strategies.
Referral to a nephrologist would appear to be preferable at the present time as
the field is advancing with new therapies being evaluated and implemented in
practice.
At the American Society of Nephrology Renal Week 2004 meeting, results
are being presented on the administration of oral paricalcitol, now in capsular
form, so that its use can be evaluated in patients with earlier stages of kidney
disease (stage III and IV), who are not yet on dialysis. The phase 3 studies of
orally administered paricalcitol showed that this strategy is effective in reducing
the degree of hyperparathyroidism, and that the administration of this vitamin D
analog is not associated with hypercalcemia, hyperphosphatemia, or
hypercalcuria. Thus, the treatment was effective and well tolerated and appeared
to be free of side effects. These studies are important because they provide a
new therapy for the complication of hyperparathyroidism in the course chronic
kidney disease, and, thus, if the diagnosis of this complication can be made
earlier in the course of chronic kidney disease, treatments such as oral
paricalcitol may be effective in managing this complication.
As nurses, we could help our patients by having a deep understanding of
the disease, that we may learn the proper interventions for the chronic kidney
disease patients. In this way, we could render quality care for them. We could as
well lead them to the proper treatment to lessen their sufferings brought by the
kidney failure, in anyhow. By having a wide understanding of the disease, we
could impart teachings on how we could prevent the occurrence of chronic
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kidney disease. As nurses, it is our responsibility to render information and impart
health teachings to improve the condition of our patients to the best of our
abilities. One of the characteristics that we, nurses, should have is to be
informative and only through a keen study of disease such as this way for us to
gain all the information that we need to learn. May this case study served its
purpose through the help of our Lord, Jesus Christ.
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B. Family Health-Illness History
Mo
Po
ma
p
Mr. Scrooge
(+) HPN
(+)Kidney
Failure
Mr. Scrooge was known for being hypertensive for 5 years now. He was
diagnosed of hypertension and kidney failure last 2001. He was hospitalized in
St. Luke’s Hospital because of the said health problem. According to him, his
chief complain that time was only hypertension. He was discharged from the
hospital after six days of confinement. After his discharge, Mr. Scrooge
consistently having his blood chemistry and creatinine check-up every month in
AUFMC. If the results are all normal, his check-up becomes every month. These
all became routine on him.
On May 2004, he was hospitalized for the second time in AUFMC. After
two days of confinement in the hospital, he decided to transfer in St. Luke’s
Hospital. Mr. Bean experienced difficulty of breathing and fatigability that time.
He was diagnosed of Pulmonary Congestion.
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D. History of Present Illness
E. Physical Examination
February 3, 2005
Upon Admission:
VS:
T - 36.8
RR - 22
PR - 64
BP - 170/100
Integumentary
A. Skin- pallor, brown in complexion, with good skin turgor
B. Nails- pallor nailbed, clean with weak capillary refill (approximately within 4
seconds)
Head-no mass palpated
A. Scalp- hair evenly distributed without any presence of lice and lesions
B. Eyes- with pale palpebral conjunctiva, no discharges noted, pupils are equally
round and reactive to light and accommodation
C. Ears- symmetrical with cerumen, no discharges noted
D. Nose- without flaring of nostrils, no discharges noted
E. Mouth- with dry and pale lips
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F. Neck- no mass palpated, without lesions, no enlargement of lymph nodes and
pain
G. Chest and Lungs- with bibasal rales
Abdomen- soft, flat, tender
February 7, 2005
Vital Signs:
T - 36
RR - 22
PR - 81
BP - 170/100
Integumentary
A. Skin- pallor, brown in complexion, with good skin turgor
B. Nails- pallor nailbed, clean with weak capillary refill (approximately within 4
seconds)
Head-no mass palpated
A. Scalp- hair evenly distributed without any presence of lice and lesions
B. Eyes- with pale palpebral conjunctiva, no discharges noted, pupils are equally
round and reactive to light and accommodation
C. Ears- symmetrical with cerumen, no discharges noted
D. Nose- without flaring of nostrils, no discharges noted
E. Mouth- with dry and pale lips
F. Neck- no mass palpated, without lesions, no enlargement of lymph nodes and
pain
G. Chest and Lungs- with bibasal rales
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Abdomen- soft, flat, tender
Cardiovascular changes: hypertension
Renal and urologic changes: oliguria
Hematopoietic changes: anemia
February 8, 2005
Vital Signs:
T - 36.2
RR - 16
PR - 80
BP - 170/100
Integumentary
A. Skin- pallor, brown in complexion, with good skin turgor
B. Nails- pallor nailbed, clean with weak capillary refill (approximately within 4
seconds)
Head-no mass palpated
A. Scalp- hair evenly distributed without any presence of lice and lesions
B. Eyes- with pale palpebral conjunctiva, no discharges noted, pupils are equally
round and reactive to light and accommodation
C. Ears- symmetrical with cerumen, no discharges noted
D. Nose- without flaring of nostrils, no discharges noted
E. Mouth- (-) pallor, dry lips
F. Neck- no mass palpated, without lesions, no enlargement of lymph nodes and
pain
G. Chest and Lungs- with bibasal rales
Abdomen- soft, flat, tender
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February 9, 2005
Vital Signs:
T - 36.4
RR - 20
PR - 71
BP - 160/100
Integumentary
A. Skin- pallor, brown in complexion, with good skin turgor
B. Nails- pallor nailbed, clean with weak capillary refill (approximately within 4
seconds)
Head-no mass palpated
A. Scalp- hair evenly distributed without any presence of lice and lesions
B. Eyes- with pale palpebral conjunctiva, no discharges noted, pupils are equally
round and reactive to light and accommodation
C. Ears- symmetrical with cerumen, no discharges noted
D. Nose- without flaring of nostrils, no discharges noted
E. Mouth- with (-) pallor, dry lips
F. Neck- no mass palpated, without lesions, no enlargement of lymph nodes and
pain
G. Chest and Lungs- with bibasal rales
Abdomen- soft, flat, tender
Renal and Urologic changes: oliguria
Cardiovascular changes: hypertension
Hematopoietic changes: anemia
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February 10, 2005
Vital Signs:
T - 37
RR - 17
PR - 85
BP - 180/90
Integumentary
C. Skin- pallor, brown in complexion, with good skin turgor
D. Nails- pallor nailbed, clean with weak capillary refill (approximately within 4
seconds)
Head-no mass palpated
H. Scalp- hair evenly distributed without any presence of lice and lesions
I. Eyes- with pale palpebral conjunctiva, no discharges noted, pupils are equally
round and reactive to light and accommodation
J. Ears- symmetrical with cerumen, no discharges noted
K. Nose- without flaring of nostrils, no discharges noted
L. Mouth- (-) pallor
M. Neck- no mass palpated, without lesions, no enlargement of lymph nodes and
pain
N. Chest and Lungs- with bibasal rales
Abdomen- soft, flat, tender
Renal and Urologic changes: oliguria
Cardiovascular changes: hypertension
Hematopoietic changes: anemia
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F. Diagnostic and Laboratory Procedures
Date Normal
Diagnostic/ Ordered Values
Indication (s) Analysis and
Laboratory Date Result used by
Purpose (s) Interpretation
Procedure Result the
in hospital
1. CBC
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Determines all above
any acute normal level.
Lymphocytes Ordered bacterial .1 This shows
2/3,4,6, infection .13 presence of
8,9/05 .20 .10-.40 bacterial
.15 infection
Result: .13
2/3,4,6,
8,9/05
Determines
Eosinophils Ordered any acute .04
2/3,4,6, bacterial .04
8,9/05 infection .05 .00-.07 Some of the
.04 results were all
Result: .06 above normal
2/3,4,6, Level
8,9/05 indicating
presence of
bacteria.
To determine
any allergic
reaction of
the body
Results were
all within the
normal level.
This shows no
allergic
reactions.
Nursing Responsibilities:
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1. Explain the procedure to the patient
2. Tell the patient that no fasting is required
3. Apply pressure or a pressure dressing to the venipuncture site
4. Assess the venipuncture site for bleeding
Diagnosti
Date
c/ Analysis and
Ordered Indication (s)
Laborator Result Interpretatio
Date Purpose (s)
y n
Result in
Procedure
Nursing Responsibilities:
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4. Handle the specimen as if it were capable of transmitting hepatitis
5. Immediately discard the needle in the appropriate receptacle
6. Send the specimen to the laboratory promptly
Normal
Date Indication Analysis
Diagnostic/ Values
Ordered (s) and
Laboratory Result used by
Date Purpose Interpretati
Procedure the
Result in (s) on
hospital
Bacteria: (-),
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few, (-)
Amorphous
urates:
Moderate,
moderate, few
Nursing Responsibilities:
Normal
Date
Diagnostic/ Indication Values Analysis and
Ordered
Laboratory (s) Result used by Interpretatio
Date
Procedure Purpose (s) the n
Result in
hospital
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4. Ordered: This test 1499 44.20- Results
Creatinin 2/3,4,6,8/0 was 1430 150.30 were all
e 5 ordered in 1649 umol/L above the
order to 731 normal level
Result in: evaluate indicating
2/3,4,7,9/0 renal renal
5 function. malfunction.
The kidney
cannot
excrete
nitrogenous
waste
product of
137 protein
135-150 leading to
5. Na+ Ordered: To mmol/L its
2/3/05 evaluate accumulatio
fluid and n in the
Result in: electrolyte blood
2/3/05 imbalance
and 4.78 Normal
identify 3.5-5.5 result which
6. K+ Ordered: renal mmol/L means
2/3,6/05 dysfunctio there is still
n fluid and
Result in: electrolyte
2/3,7/05 To balance
evaluate 6.4
fluid and 8.5-10.5
7. Ordered: electrolyte mg/dl Normal
Calcium 2/3/05 imbalance result which
and means
Result in: identify there is still
2/3/05 renal fluid and
dysfunctio electrolyte
n 186 balance
30-150
Ordered: To u/L
8. 2/3/05 evaluate Results
Phosphat muscle were all
e Result in: contraction above the
2/3/05 , nerve normal level
impulse indicating
transmissi renal
on, and malfunction.
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blood
clotting
To Results
evaluate were all
the above the
metabolis normal level
m of indicating
carbohydra renal
tes, bone malfunction.
formation
and acid-
base
balance.
Nursing Responsibilities:
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2.Tell the patient that no fasting is required
3. Apply pressure or a pressure dressing to the venipuncture site
4. Assess the venipuncture site for bleeding
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Kidneys
The kidneys balance the urinary excretion of substances against the
accumulation within the body through ingestion or production. Consequently,
they are major controller of fluid and electrolyte homeostasis. The kidneys also
have several non-excretory metabolic and endocrine functions, including blood
pressure regulation, erythropoietin production, insulin degradation, prostaglandin
synthesis, calcium and phosphorus regulation and Vitamin D metabolism.
The kidneys are located retroperitoneally, in the posterior aspect of the
abdomen. On either side of the ventral column. They lie between the 12 th thoracic
and third lumbar vertebrae. The left kidney is usually positioned slightly higher
than the right. Adult kidneys are average approximately 11 cm in length, 5 to 7.5
cm in width, and 2.5 cm in thickness. The kidney has a characteristic curved
shape, with a convex distal edge and a concave medial boundary.
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vertebra, enter the kidney, and progressively branch into lobar arteries. Blood
flows from the interlobular arteries through the afferent arteriole, the glomerular
capillaries, the efferent arteriole and the peritubular capillaries. Some of the
peritubular capillaries carry a small amount of blood to the renal medulla in the
vasa recta before entering the venous drainage. The blood leaves the kidney in
venous system closely corresponding to the arterial system: interlobular veins,
arcuate veins, interlobar veins, and the renal vein. The renal circulation then
empties into the inferior vena cava.
Physiology
Characteristics of Urine
Urine is a watery solution of nitrogenous waste an inorganic salts that are
removed from the plasma and eliminated by the kidneys. It is 5% water and 5%
dissolved solids and gases. The amount of these dissolved substances is
indicated by it specific gravity. The specific gravity of pure water, used as a
standard is 1.000. Because of the dissolved materials it contains, urine has a
specific gravity that normally varies from 1.010 to 1.040. When the kidneys are
diseased, they lose the ability to concentrate urine, and the specific gravity no
longer varies as it does when the kidneys function normally.
Urine formation
The chief function of the kidneys is to produce urine. Each part of the
nephrons performs a special function. There are three important processes by
which urine is formed. They are glomerular filtration, tubular reabsorption and
tubular secretion
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Electrolytes must be kept in the proper concentration in both intracellular and
extracellular fluids. Although some electrolytes are lost in the feces and through
the skin as sweat, the job of balancing electrolytes is left mainly to the kidneys.
There are several hormones that are involved in this process. Aldosterone
produced by the adrenal cortex promotes the reabsorption of sodium and the
elimination of potassium. Hormones from parathyroid and thyroid glands regulate
calcium and phosphate levels. Parathyroid hormones increases blood calcium,
levels by causing the bones to release calcium and by causing the kidneys to
reabsorb calcium. The thyroid hormone calcitonin lowers blood calcium by
causing calcium to be deposited in the bone.
Precipitating Factors
Chronic glomerular disease such as glomerunephritis
Chronic infections such as chronic pyelonephritis or tuberculosis
Congenital anomalities such as polycystic
Vascular diseases, such as renal nephrosclerosis or hypertension
Obstructive processes such as calculi
Collagen diseases such as systemic lupus erythematosus
nephrotoxic agents such as long-term aminoglycoside
endocrine diseases such as diabetic neuropathy
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Such conditions gradually destroy the nephrons and eventually cause
irreversible renal failure. Similarly, acute renal failure that fails to respond to
treatment becomes chronic renal failure.
Predisposing Factors
Sex- both sexes are affected by chronic renal failure. But in 1998, based on
United States Renal Data System, a higher total number of males with ESRD
was found
Age- CRF can be found in people of any age, from infants to the very old.
The elderly population also is the most rapidly growing ESRD population in
the United States. Note that age 30 years progressive physiological
glomerulosclerosis. Aging also results in concomitant progressive
physiological decrease in muscle mass such that daily urinary creatinine
excretion also decreases.
Clinical Manifestations
The clinical manifestations of CRF are present throughout the body. No
organ system is spared.
Electrolyte imbalances
Electrolyte balance may be upset by impaired excretion and
utilization in the kidney. Although many clients maintain normal serum
sodium level, the salt-wasting properties of some failing kidneys, in
addition to vomiting and diarrhea, may cause hyponatremia. Because the
kidneys are efficient at excreting potassium, potassium levels usually
remain within normal limits until late in the disease.
Several mechanisms contriburte to hypocalcemia. Conversion of
25-hydroxycholecalciferol to 1,25-dihyroxycholecalciferol (necessary to
absorb calcium) is decreased, which results in reduced intestinal
absorption of calcium. At the same time, phosphate is not excreted, which
causes hyperphosphatemia. Because calcium and phosphate are
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inversely related, a high phosphate level results in a reduced calcium
level.
Metabolic changes
In advancing renal failure, BUN and serum creatinine rise as waste
products of protein metabolism accumulate in the blood. The serum
creatinine level is the most accurate measure of renal function. The
proteinuria accompanying renal disease and sometimes inadequate
dietary intake of proteins cause hypoproteinuria, which lowers the
intravascular oncotic pressure. Metabolic acidosis occurs because of the
kidney’s inability to excrete hydrogen ions. Decrease reabsorption of
sodium bicarbonate and decreased formation of dihydrogen phosphate
and ammonia contribute to this problem. Acidosis accentuates
hyperkalemia and the reabsorption of calcium from the bones.
Hematologic changes
The primary hematologic effect of renal failure is anemia, usually
normochromic and normocytic. It occurs because the kidneys are unable to
produce erythropoietin, a hormone necessary for red blood cell production.
Frequently, the fatigue, weakness, and cold intolerance accompanying the
anemia lead to a diagnosis of renal failure.
Gastrointestinal changes
The entire gastrointestinal system is affected. Transient anorexia,
nausea, vomiting are almost universal. Clients often experience a constant
bitter , metallic, or salty taste, and their breath commonly smells fetid, fishy or
ammonia-like. Stomatitis, parotitis and gingivitis are common problems
because of poor oral hygiene and the formation of ammonia from salivary
urea. Accumulations of gastro may be a major cause of ulcer disease.
Esophagitis, gastritis, colitis, gastrointestinal bleeding, and diarrhea may be
present. Serum amylase level may be increased, although they do not
necessarily indicate pancreatitis.
Immunologic changes
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Impairment of the immune system makes the client more susceptible
to infection. Several factors are involved, including depression of humoral
antibody formation, suppression of delayed hypersensitivity and decreased
chemotactic function of leukocytes. Immunosuppression is an important part
of the medical management of renal diseaes such as glomerulonephritis.
Cardiovascular changes
The most common clinical manifestation is hypertension, produced
through:
mechanism of volume overload, stimulation of the renin-angiotensin system,
sympatheically mediated vasoconstriction, absence of prostaglandins.
Respiratory changes
Some of the respiratory effects such as pulmonary edema can be
attributed to fluid overload. Metabolic acidosis causes a compensatory
increase in respiratory rate as the lungs try to eliminate excess hydrogen
ions.
Musculoskeletal changes
The etiologic mechanism involves the kidney-bone-parathyroid and
calcium-phosphate-vitamin D connections. As the GRF decreases, the
phosphate excretion decreases and calcium elimination increases. Abnormal
levels of calcium and phosphate stimulate the release of parathyroid hormone
that mobilizes calcium from the bones and facilitates phosphate excretion.
Integumentary changes
The skin is also often very dry because of atrophy of the sweat glands.
Severe and intractable pruritus may result from secondary
hyperparathyroidism and calcium deposits in the skin. The pallor of anemia is
evident.
A. Medical Management
Medical Date General Indication Client’s Client’s
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initial
ordered response
Manageme (s) reaction to
Date Description to the
nt Purpose (s) the
performed treatment
treatment
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two-way chilling for some
flow of a short reaction
blood To period of such as
immediatel time. chilling but
It is y restore There was there was
intravenou blood no further not further
s volume to adverse reaction
replaceme treat reaction after the
Ordered: nt of loss severe noted upon treatment
2/7,8,9/05 or anemia, to the
5. destroyed be able to transfusion
Hemodial Performed: blood maintain
ysi 2/7,8,10/0 compatible oxygen
s 5 citrated transport
human to the Patient
blood it is different was
also the parts of slightly There was
introductio the body nervous no adverse
n of whole about the reaction
blood or treatment noted
blood . during and
Componen after the
t procedure
It is
indicated
for the
Medical patient
treatment because
used to the
promote kidneys
excretion cannot
of wastes function
materials very well
from the to excrete
blood of the
patient. nitrogenou
s waste
products,
thus
leading to
its
accumulati
on in the
blood.
Nursing Responsibilities
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1. Blood transfusion
Before
a. Assess client for history of previous BT and any adverse reactions
b. Ensure that the client has an 18 to 19 gauge IV catheter in place
c. Use 0.9% sodium chloride IVF
d. Verify the ABO group, Rh type, client and blood numbers and expiration
date.
e. Take baseline vital signs before initiating BT
f. Identify the patient prior to transfusion
g. Explain the purpose of the transfusion
During
a. Start transfusion slowly
b. Maintain prescribed transfusion rate
c. Monitor patient closely. Check vital signs every 15 mins. Until 2 hours post
transfusion
After
a. Monitor for adverse reactions
b. Documentation
2. Hemodialysis
Before
a. Explain the purpose of the transfusion
b. Have client void
c. Chart client’s weight
d. Withhold antihypertensive, sedatives, vasodilators, to prevent hypotension
(unless ordered otherwise)
During
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a. Obtain and record vital signs before and every 30 mins. during the
procedure
b. Ensure bedrest with frequent position changes for comfort
c. Proper heparinization must be done to prevent coagulation during the
therapy
d. Inform client that headache and nausea may occur
e. Monitor closely for bleeding since blood has been heparinized for
procedure
After
a. Weight the patient after the therapy and record
b. Monitor vital signs especially hypotension.
c. Assess for complications (hypovolemic shock, dialysis disequilibrium
syndrome)
Date
ordered Route of
Client’s
Date admin. Indication
Name of General response
Taken Dosage (s)
Drug action to
Date and freq. Purpose(s)
medication
changed or Of admin.
D/C
Amlodipi Ordered:
ne 2/3/05
besylate
Taken: PO 5 mg Calcium To Patient did
antagonist,
• norvas 2/3-10/05 decrease not show
OD antihyperte
nsive
increase any side
c blood effects
pressure
Metoprol Ordered:
ol tartate 2/3/05 Beta Patient did
PO 50 mg blockers, To decrease not show
• neoblo Taken: OD antihyperte increase any side
2/3-10/05 nsive drug blood effects
c pressure
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Ordered:
2/3/05
Iron Patient’s
stool was
Taken: PO 1 cap deficiency
For patient dark green
Iberet- 2/3-10/05
BID having in color
folic acid
anemia
changed:
2/3/05
Ordered:
2/3/05
Patient did
not show
furosemi Taken: Diuretic
any side
2/3-10/05
de PO 40 mg For oliguric effects
patient
• lasix OD
Ordered:
2/3/05
Taken:
Patient did
2/3-10/05 Calcium
To treat not show
supplemen
calcium PO 1 tab. hypocalce any side
D/C: t
carbonat mia effects
2/3/05 TID
e
Nursing Responsibilities
Prior:
1. Check and determine the prescribed the drug.
2. Inform the patient about the prescribed the drug.
3. Explain the procedure, purpose, indication and side effects of the drug.
During:
1. Check vital signs to obtain baseline data.
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2. Monitor BP
3. Prepare the drug and the materials
4. Observe for initial assessment.
5. Observe for any initial response to the treatment.
After:
1. Observe for any intolerance and side effects on the prescribed drug.
Nursing Responsibilities
Prior:
1. Check and determine the prescribed diet
2. Inform the SO about the prescribed diet
3. Explain the procedure and purpose of the prescribed diet
4. Cite foods that are restricted.
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During:
1. Check vital signs to obtain baseline data
2. Observe for initial response.
After:
1. Inform SO if it would be changed
2. Observe and monitor for changes
Nursing Responsibilities
B. Surgical Management
Arteriovenous Fistula
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A surgeon creates an AV fistula by connecting an artery directly to a vein,
usually in the forearm. Connecting the artery to the vein causes more blood flow
into the vein. As a result, the vein grows larger and stronger, making repeated
insertions for hemodialysis treatment easier. For the surgery, you will be given a
local anesthetic. In most cases, the procedure can be performed on an outpatient
basis.
Nursing management
Actual SOAPIE
February 3, 2005
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>VS taken and recorded as follows: T-36, PR-64, RR-18, BP-150/90
Actual SOAPIE
S>
O> received patient on supine position, awake, afebrile with pale conjunctiva,
appears weak with easy fatigability
> VS taken and recorded as follows: T-36, PR-90, RR-16, BP-170/90
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P > after 6 hrs of nursing interventions, patient will improve cardiac output as
evidence by normal vital signs and decreased in paleness and fatigability
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BP 150/ 160 140 170 17 170 160 180/
90 / / / 0/1 / 90 / 90
100 80 80 10 100
C. Diagnostic Procedures
1. CBC
2. Creatinine
3. Urinalysis
4. Hepatitis profile
D. Medical Management
1. D5 LRS 1 L
2.D5 NaCl
3. Blood transfusion
4. Hemodialysis
5. Subclavian catheterization
E. Drugs
1. Norvasc
2. Neobloc
3. Iberet +Folic
4. Calcium carbonate
5.furosemide
F. Diet
1. DAT
2. Low salt low protein
G. Activity / Exercise
1. Bed rest
B. Discharge Planning
Mr. Scrooge was discharge last February 10, 2005, Upon discharged, Mr.
Scrooge’s physical appearance was improved. There was absence of paleness
in the conjunctiva and lips, fatigability is decrease, and with decrease creatinine
level as compared when he was admitted in the hospital. His vital signs were as
follows: T- 36.5, PR- 85, RR-18, BP- 140/100.
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Mucosolvan 1 tsp. TID
Augmentin 375 mg 1 tab TID
Nifedipine lozenges QID
>For twice a week hemodialysis
E>Bed rest
T>proper wound care (subclavian and fistula)
H>strict compliance to the medications and in hemodialysis
O>follow-up check up on February 15, 2005
D>avoid foods rich in salt and protein
>Limit fluid intake
VIII. Bibliography
37
Philadelphia
Handbook of Diseases. (1999) 2nd edition.. Springhouse Corporation
Springhouse, Pennsylvania
Pagana (2002). Mosby’s Manual of Diagnostic and Laboratory Tests.
MIMS. (2003)
www.yahoo.com
www.google.com
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