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OUR LADY OF FATIMA

UNIVERSITY
COLLEGE OF NURSING
VALENZUELA CAMPUS

Anemia Unspecified

In Partial Fulfillment of requirements of NCM 107B RLE leading to the degree


of Science in Nursing

Presented to:
Mr. Fred Ruiz
Presented by:
Bungay, Maria Paula M.
BSN 4Y 2-1
Group 1B
August 28, 2015

TABLE OF CONTENTS

I. Introduction
II. Objectives
III. Patients Profile
IV. Anatomy and Physiology
V. Pathophysiology
VI. Laboratory Examination Results
VII. Gordons Assessment
VIII. Nursing Care Plans
IX. Drug Study
X. Health Teachings

I. INTRODUCTION
The main function of a red blood cell or erythrocyte is to carry and
transport oxygen to the different parts of the body. The normal RBC count is
4-6 million/mm3. Hemoglobin (Hgb), an iron-bearing protein, is found inside
an erythrocyte. Molecules of this iron containing protein are responsible for
transporting the bulk of oxygen that is carried in the blood.
The more hemoglobin molecules the RBC contain, a higher amount of oxygen
will they be able to carry. If the hemoglobin is defective, the erythrocyte will
also malfunction. A red blood cell is just a vessel; the one that performs the
oxygen transportation is the hemoglobin. Normal hemoglobin is 13-18
grams/dl in males and 12-16 grams/dl in females. A decrease in the RBC or
hemoglobin or the oxygen-carrying ability of a blood is termed as anemia.
Erythrocyte Formation
RBCs are produced by the bone marrow a process known as erythropoiesis.
Before a red blood cell is formed, the hematopoietic stem cell first produces
an uncommitted stem cell to be formed to committed progenitor cell.
Progenitor cells are not only the precursor of RBC, but also of lymphocytes
and megakaryocytes (antecedent of platelets). Before an erythrocyte is
formed the progenitor cells develop an erythroblast, then a reticulocyte, and
finally erythrocyte (RBC). A hormone, erythropoietin, which is secreted by the
kidney, also controls RBC production by stimulating the bone marrow.
Types of anemia
Hypoproliferative Anemias
This type of anemia covers all condition where the bone marrow incapable of
producing enough cells to develop to erythrocyte. Lack of erythropoietin may
also be a contributing factor of the abnormality. The following types of
anemia are under this classification:

Aplastic anemia In this condition, the precursor cells (stem or


progenital cells, which is responsible in forming components of blood)
are extremely deficient, thereby, production of all formed elements
(including RBC, lymphocyte, megakaryocytes) are reduced. Because of
the depressed bone marrow function, it is replaced by fat cells leading
to anemia, excessive bleeding (thrombocytopenia) and infections
(depressed WBC count). This type of anemia is also a common
example of a pancytopenic disorder.

Iron-deficiency anemia It is also called microcytic, hypochromic


anemia. This is type of anemia is the most common form among all
ages, and is characterized by a low iron concentration in the body.

Megaloblastic anemia A macrocytic, normochromic anemia results as


the essential factors (vitamin B12 and folic acid) for normal DNA
synthesis are missing causing suppression of mitosis in the bone
marrow and allowing the RNA or protein synthesis to take place for the
progression of cell growth without cell division. The resulting cells
remain enlarged (because mitosis is absent).

1. 1. Vitamin B12 deficiency Vitamin B12 or cobalamin is required


for normal DNA synthesis. It is not synthesized in the tissues of but
solely depends on the dietary intake of meat, liver, dairy products and
sea foods.
2. 2. Folic Acid Deficiency folic acid is also important for the DNA
synthesis of cells. The dietary sources of folate are meats, eggs, leafy
vegetables which are easily available.
Hemolytic Anemias
This type of anemia refers to the state where hemolysis(erythrocyte
destruction) causes symptoms of anemia. Classification of this condition is
further narrowed into intrinsic (inherited) or extrinsic (damage in erythrocyte
is caused by environmental factors).

Intrinsic Hemolytic Anemia

1. Sickle Cell anemia an inherited disorder on the beta chain of the


hemoglobin resulting to abnormally shaped red blood cells. In this
condition an abnormal hemoglobin S (HbS) is contained in the RBCs
causing distortions or sickling of the red blood cells.
2. Thalassemia group of genetic disorders that involve a defective
hemoglobin- chain synthesis. Thalassemia majoris threatening disease
characterized by severe anemia, hemolysis and ineffective
erythropoiesis. Thalassemia minor is a mild form of anemia. The
affected individual has only one defective gene and is asymptomatic.

Extrinsic Hemolytic Anemia

1. Immune hemolytic anemia a persons own antibodies destroy his own


red blood cells (hemolysis).

2. Mechanical hemolytic anemia hemolysis is caused by trauma or


physical injuries that disrupt red blood cells altering and tearing them
through the small vessels.

II. OBJECTIVES
Nurse Centered
1. Describe factually, the personal and pertinent family history of the
patient and relate it to the present condition.
2. Perform comprehensive physical assessment.
3. Trace the book-based and client-centered pathophysiology
4. Determine the predisposing and precipitating factors and the signs and
symptoms and relate to the disease process.
5. Enumerate and describe the diagnostic and laboratory procedures as well
as the nursing responsibilities in relation to the disease condition
6. Enumerate the different treatment modalities and their indication
specifically for the patients condition.
7. Identify the pharmacologic treatment provided to the patient, relate the
actions of each drug with the disease process and evaluate the patients
response to the medications given.
8. Identify nursing diagnoses, formulate short-term goals, carry out
appropriate interventions and evaluate the plan.
9. Appraise the effectiveness of medical and surgical nursing management
in treating the patient.
10. List the preventive measure for the occurrence of Anemia.
Patient Centered
1. Report understanding of the disease process.
2. Understand the indications of the different diagnostic procedures and
medical management involved in her care.
3. Cooperate with the necessary medical and nursing interventions.
4. Adhere with the health teachings provided.
5. Understand the different ways of health promotion and prevention in
relation to the disease condition.
6. Demonstrate improved conditions as evidenced by absence of further
complications.

III. PATIENT'S PROFILE

Name: MS. AC
Age: 16 years old
Nationality: Filipino
Religion: Roman Catholic
Civil Status: Single
Date Admission: August 16, 2015
Time of Admission: 10:54 PM
Ward: Pediatric Ward
Initial Diagnosis: Blood Dyscrasia probably ALL
Diagnosis: Anemia, Unspecified
HISTORY OF PAST ILLNESS
Ms. AC usually had conditions such as coughs and colds as well as
fever, which they treated, as stated by her father, by giving her BIOGESIC or
other over the counter drugs. Father stated that she already experienced
serious infections such as chickenpox and measles. The last time she was
admitted to the hospital was June 15, 2015. Ms. AC has no family history of
Anemia. She has no known food and drug allergies. Ms. Ac is not fond of
eating meat and vegetables and she would often miss her mealtime. At the
young age she started working as a maid and stop going to school due to
financial problem. As stated by Ms. AC her sleeping pattern is usually at 2
A.M.
PHYSICAL ASSESSMENT
Physicians Physical Assessment done by the Resident on Duty (August
16, 2015), lifted from the patient's chart)
Height: 59 cm
Weight: 41 kg
Vital Signs as follows:
T: 36.6C

PR: 112 bpm

RR: 42cpm

BP: 110/60 mmHg

SAO2: 98%

GENERAL SURVEY
Ms. AC, Assessed/received patient lying on bed, sleeping, conscious
with GCS 15. With the following vital signs:
Temperature: 36.6 C
Heart rate: 112 bpm
Respiratory rate: 20 bpm
Blood Pressure: 110/70 mmHg
SAO2: 99%

IV. ANATOM Y AND PHYSIOLOGY


The production of red blood cells is referred to as erythropoiesis.
Mature red blood cells develop from hemocytoblasts. This development takes
about 7 days and involves three to four mitotic cell divisions, so that each
stem cell gives rise to 8 or 16 cells. The various cell types in erythrocyte
development are characterized by the gradual appearance of hemoglobin
and

disappearance

of

ribonucleic

acid

(RNA)

in

the

cell

the progressive degeneration of the cell's nucleus which is eventually


extruded from the cell the gradual loss of cytoplasmic organelles, for example
mitochondria

gradual

reduction

in

cell

The young red cell is called a reticulocyte because

size.
of a network

of ribonucleic acid (reticulum) present in its cytoplasm. As the red cell


matures the reticulum disappears. Between 2 and 6% of a newborn baby's
circulating red cells are reticulocytes, but this reduces to less than 2% in the
healthy adult. However, the reticulocyte count increases considerably in
conditions

in

which

rapid erythropoiesis occurs, for example following hemorrhage or acute


hemolysis of red cells. A reticulocyte normally takes about 4 days to mature
into an erythrocyte. In health, erythropoiesis is regulated so that the number
of circulating erythrocytes is maintained within a narrow range. Normally, a
little less than l% of the body's total red blood cells are produced per day and
these replace an equivalent number that have reached the end of their life
span.

However

that

still

represents

huge

200,000,000,000

cells.

Erythropoiesis is stimulated by hypoxia (lack of oxygen).


However, oxygen lack does not act directly on the hemopoietic tissues
but

instead

stimulates

the

production of a hormone,

erythropoietin.

This hormone then stimulates hemopoietic tissues to produce red cells.


Erythropoietin is a glycoprotein. It is inactivated by the liver and excreted in
the urine. It is now established that erythropoietin is formed within the kidney
by the action of a renal erythropoietin factor erythrogenin on plasma protein,
erythropoietinogen. Erythrogenin is present in the juxtaglomerular cells of the
kidneys and is released into the blood in response to hypoxia in the renal
arterial

blood

supply.

Various other factors can affect the rate of erythropoiesis by influencing

erythropoietin production. Thyroid hormones, thyroid-stimulating hormone,


adrenal cortical steroids, adrenocorticotrophic hormone, and human growth
hormone

(HGH)

all

promote

erythropoietin formation and so enhance red blood cell formation


(erythropoiesis). In thyroid deficiency and anterior pituitary deficiency,
anemia may occur due to reduced erythropoiesis.
Polycythemia (excess red blood cell production) is often a feature
of Cushing's syndrome. However, very high doses of steroid hormones seem
to

inhibit

erythropoiesis.

Androgens (male hormones) stimulate and estrogens (female hormone


s) depress the erythropoietic response. In addition to the effects of menstrual
blood loss, this effect may explain why women tend to have a lower
hemoglobin concentration and red cell count than men. Plasma levels of
erythropoietin are raised in hypoxic conditions (low oxygen levels).
This produces erythrocytosis (increase in the number of circulating
erythrocytes) and the condition is known as secondary polycythemia. A
physiological secondary polycythemia is present in the fetus (and residually
in the new-born) and in people living at high altitude because of the relatively
low partial pressure of oxygen in their environment. Secondary polycythemia
occurs as a result of tissue hypoxia in diseases such as chronic bronchitis,
emphysema

and

congestive

cardiovascular

abnormalities

associated with right-to-left shunting of blood through the heart, for example
Fallot's of tetralogy. Erythropoietin is also produced by a variety of tumors of
both renal and other tissues. The oxygen carrying capacity of the blood is
increased in polycythemia but so is the thickness (viscosity) of the blood. The
increased viscosity produces circulatory problems such as raised blood
pressure. There is a condition known as primary polycythemia (polycythemia
rubra vera), where there are increases in the numbers of all the blood cells,
and plasma erythropoietin levels are normal. The cause of this condition is
unknown. The underlying cause of secondary polycythemia is treated with
the

aim

of eliminating hypoxia. Vene

section (blood letting) is sometimes employed to


reduce red cell volume to normal levels. Frequently blood is removed,
centrifuged to remove cells and the plasma returned to the patient
(plasmapheresis). In anemia there is a reduction in blood hemoglobin

concentration

due

to

decrease in the number of circulating erythrocytes and/or in the amount of he


moglobin they contain. Anemia occurs when the erythropoietic tissues cannot
supply enough normal erythrocytes to the circulation. In anemia due to
abnormal red cell production, increased destruction and when demand
exceeds capacity, plasma erythropoietin levels are increased. However,
anemia can also be caused by defective production of erythropoietin as, for
example, in renal disease.
A. Definition
Anemia is a condition where red blood cells are not providing
adequate oxygen to body tissues. Red blood cells provide oxygen to body
tissues. There are many types and causes of anemia.
B. Causes
Anemia is caused by many different things at it has a lot of subtypes.
However, the main presenting factor is the lack of healthy circulating red
blood cells to carry oxygen systemically. Here is a quick overview of the
different subtypes of anemia:
1. Iron Deficiency Anemia
Iron is needed for healthy production of red blood cells. Iron is a building
block of healthy red blood cells. A deficiency in iron would result in immature,
microsomic, and hypochromic red blood cells. Also, fewer RBCs will be
produced by the marrow. This type of anemia is the most common type of
anemia.
2. Folic-Acid Deficiency Anemia
Folate is also known as Folic Acid. This type of anemia results from a
deficiency of this B vitamin. This particular type of anemia is particularly
common among pregnant women as the developing fetus uses up the
mothers folate stores. In folate deficiency anemia, the red blood cells are

macrosomic and are called megalocytes or megaloblasts. This is the reason


why this form of anemia is called Megaloblastic Anemia
3. Thalassemia
Thalassemia is a form of anemia that is inherited. In this type of anemia, the
body makes an abnormal form it hemoglobin, the major protein in RBCs that
carry oxygen. In alpha-thalassemia, the genes related to alpha globin are
mutated or are missing. In beta thalassemia, a gene defect also affects the
production of beta globin. Thalassemia major is categorized if you inherit the
genetic defect from both parents. If only one parent however transmits the
defect, it is termed Thalassemia minor. Both conditions result to an abnormal
form of hemoglobin and leads to excessive RBC destruction leading to
anemia.
4. Vitamin B12 Deficiency Anemia
This form of anemia is due to lack of sufficient cyanocobalamin or
Vitamin B12. This type of anemia results to macrocosmic, hypochromic RBCs.
This is often referred to as Pernicious anemia. The cause of this type of
anemia could be a dietary deficiency, or a disease that impairs its proper
absorption such as Celiac disease or Crohns disease.
5. Hemolytic Anemia
Hemolytic Anemia is a type of anemia that results from excessive lysis or
destruction of RBCs. This type of anemia has a lot of causes and it also has
different subtypes. The destroying factor may be intrinsic, or extrinsic,
depending on the specific cause. In this type of anemia, RBCs are rapidly
destroyed, resulting to a low number of oxygen-carrying RBCs leading to
anemia. This type of anemia does not occur though if the bone marrow is
capable of producing much more RBCs than those destroyed.
6. Aplastic Anemia

In Aplastic anemia, there is a deficiency in sufficient production of red blood


cells by the bone marrow. There are two types of this: idiopathic, or
secondary. In idiopathic aplastic anemia, there is no clear cause as to why the
bone marrow is unable to produce new, mature red blood cells. In secondary
aplastic anemia, the failure results as a sequel from another disorder such as
renal disease (where there is decreased erythropoietin), chemotherapy,
radiation, and others.
7. Sickle-Cell Anemia
This type of anemia is caused by a particular type of hemoglobin called
hemoglobin S. Hemogloin S changes the shape of red blood cells especially
during times of low oxygen saturation of the blood. Hemoglobin S causes
cells to become shaped like sickles or crescents. These RBCs are unable to
properly carry oxygen, and they often get lodged into capillaries and block
them.
C. Symptoms
Symptoms of anemia may vary from the specific subtype, but these are some
of the general signs and symptoms:

Fatigue

Pallor

Cyanosis

Low hematocrit and RBC levels on a Complete Blood Count

Chest pain

Dizziness and Headaches

Paresthesia

Skin mottling

Shortness of Breath

Confusion and restlessness

Cold hands and feet

Tachycardia

D. Management

Management of anemia depends on the specific deficiency or the specific


subtype. Nonetheless, conventional management includes:
1. Supplementation with Iron, Folate, or Vitamin B 12
2. Use of corticosteroids in anemias where there is destruction of
RBCs
3. Blood Transfusions
4. Erythropoietin supplementation
5. Rest
6. Treatment of the underlying condition that causes the anemia
E. Prevention
Prevention of anemia is possible. Ensuring that you eat a proper diet is one of
the keys towards prevention of this disease. Supplement your diet with foods
rich in iron, folate, vitamin B12 and vitamin C such as green leafy vegetables,
dairy, eggs, organ meats, lentils, beans, meat, and others. If there is an
underlying medical condition that may cause anemia, consult your doctor as
to how to manage this condition.

V. PATHOPHYSIOLOGY
Anemia Schematic Diagram

Predisposing Factors
-Sex (menstruation)
-Genetics

Precipitating Factors
-Inadequate Iron intake &
faulty diet
-Blood Loss
-Pregnancy

Decreased intake of iron


rich foods, with blood
loss

Iron in the body is used


up
Decreased iron reserves
needed for hemoglobin
production

Decreased RBC
production due to lack of
hemoglobin
Iron Deficiency Anemia

Decreased oxygen and


hemoglobin

Pallor due to
decreased hemoglobin

Headache due to
decreased oxygen supply
to the brain

Weakness due to
decreased overall oxygen
supply

If prolonged:
*Chest Pain (Lack of oxygen in the heart)
*Shortness of Breath even with rest
*Paresthesia (indicates nerve affectation)
*Disorientation and Confusion (if the
brain is severely deprived of oxygen)
*Low RBC and Hematocrit levels

VI. LABORATORY EXAMINATION RESULTS

VII. GORDON'S ASSESSMENT


A. Health Perception and Management
o Client cant recall well if he was completely immunized.
o Client was brought to the hospital for management.
B. Nutrition/ Metabolism
o Fond of eating meats and fruits
C. Elimination
o Voids usually 5 times a day
o Urine color is yellow
o Defecates usually every other day.
D. Activity/Exercise
o Bedrest with semi-fowlers position.
o Minimal movements
E. Sexuality/Reproductive
o Single
o No history of STDS
F. Cognitive/Perceptual
o Is not oriented to time due to post-op surgery.
o Responds to stimuli physically.
o Undergrad
o Not in a normal thought process due to condition and surgery.
G. Roles/Relationship
o Single
o Well-supported by the family
H. Self-Perception/ Self-Concept
o Hopeful to be relieve and treated
o Manages healthy lifestyle before his condition
I. Value/Belief
o Born Again Christian
o Has a strong faith in God
J. Coping/ Stress
o S/P VPS in 2013
o Copes up with problems
K. Sleep/Rest
o Difficulties in sleeping
o Not enough rest intervals
L. Medication History
o Meds for his previous hospitalization in 2013

VIII. NURSING CARE PLAN


#1
ASSESSMENT

DIAGNOSIS

Subjective:
Nanghihina
ako,kadalasan
hindi ko matapos
ang mga gawain
ko
(Im feeling weak,
I cant even
complete my
chores
) as verbalized
by the patient.

Objective:
Fatigue.

Greater need

Activity
intolerance
related to
imbalance
between oxygen
supply (delivery)
and demand.

OBJECTIVE

INTERVENTION

RATIONALE

Short term:

Independent:

After 8 hours of
nursing
interventions the
patient will:

Assess patients
ability to perform
normal task or
activities of daily
living.

Influences
choice of
interventions or
needed
assistance.

Note changes in
balance/ gait
disturbance,
muscle
weakness.

May indicate
neurological
changes
associated with
vitamin B12
deficiency,
affecting patient
safety or risk of
injury.

Report an
increase in
activity tolerance
including
activities of daily
living.

Demonstrate a
decrease in
physiological
signs of
intolerance.

Recommend
quiet
atmosphere, bed
rest if indicated.

Enhances rest to
lower bodys
oxygen
requirements,

EVALUATION

Patient reveals
an increase in
activity tolerance,
demonstrating a
reduction in
physiological
signs of
intolerance and
laboratory values
within normal
range.

for sleep and


rest.
Display
laboratory
V/S taken as
follows: T: 36.9
P: 75 R: 18 BP:
100/80

values within
acceptable
range.

Long term:

Elevate the
head of the bed
as tolerated.

and reduces
strain on the
heart and lungs.

Provide or
recommend
assistance with
activities or
ambulation as
necessary,
allowing patient
to do as much as
possible.

Enhances lung
expansion to
maximize
oxygenation for
cellular uptake.

After months of
nursing
interventions, the
patient:

Although help
may be
necessary, self
esteem is
enhanced when
patient does
some things for
self.

Is free form
weakness and
risk for
complications
has been
prevented.
Plan activity
progression with
patient, including

Promotes
gradual return to

activities that the


patient views
essential.
Increase levels of
activities as
tolerated.

normal activity
level and
improved muscle
tone or stamina
without undue
fatigue.

Identify or
implement
energy saving
technique like
sitting while
doing a task.

Encourages
patient to do as
much as possible,
while conserving
limited energy
and preventing
fatigue.

Collaborative:
Monitor
laboratory
studies. Hb or Hct
and RBC count,
arterial blood
gases (ABGs).

Identifies
deficiencies in
RBC components
affecting oxygen
transport and
treatment needs
or response to
therapy.

IX. DRUG STUDY

NAME
NAME OF
OF
DRUGS,
DRUGS,
GENERIC
GENERIC
NAME,
NAME, BRAND
BRAND
NAME
NAME

Generic name:
Generic name:
Paracetamol
Furosemide
Brand name:
Brand name:
Calpol
Lasix

DATE
DATE
ROUTE
ROUTEOR
OR
ORDERED,
ORDERED,
ADMINISTRATI
ADMINISTRATI
DATE
DATE
ON
ONDOSAGE
DOSAGE
TAKEN/GIVEN,
TAKEN/GIVEN,
AND
AND
DATE
DATE
FREQUENCY
FREQUENCYOF
OF
CHANGED
CHANGED
ADMINISTRATI
ADMINISTRATI
ON
ON
Dosage:
Dosage:
DO: August 26, 600mg
DO: August 26, 20mg
2015
2015
DG: July 16,-21, Route:
DG: July 16,-21, Route:
2015
Oral
2015
IV
Frequency:
Frequency:
q 4hrs
mid and post
BT

GENERAL
ACTION,
GENERAL
MECHANISM
ACTION,
OF ACTION
MECHANISM
OF ACTION
General Action:
Furosemide
Analgesics
inhibits
Muscle
absorption of
Relaxants
sodium and
chloride from the
Mechanism of
proximal and
Action:
distal tubules
-Decreases fever
and ascending
by inhibiting the
limb of the loop
effects of
of henle. Leading
pyrogens on the
to a sodium rich
hypothalamus
diuresis, thus
heat regulating
reducing edema
centers & by a
associated to
hypothalamic
renal disease
resulting to
-Action leading
decrease BP.
to sweating &
vasodilatation.

INDICATION
OR
INDICATION
PURPOSES
OR
PURPOSES

CLIENTS
RESPONSE TO
CLIENTS
THE
RESPONSE
MEDICATION
TO THE
MEDICATION

Relief of mild- Clients


Indicated for The patient
to-moderate
response to
the patient as improves her
pain;
medication is
he
has condition as he
treatment of effective as
elevated
had a
fever.
evidence by
blood
decreased BP
lowering down
pressure and after 30 mins.
the patients
edema.
of
temperature
administration.

Nursing Responsibilities
Before:
Observe 10 Rs of administration of drugs '
Check doctors order three times and verify the patient
Check the label of the drug, its name and its expiration date
Wash hands before handling the medication
Assess patients vital signs prior to administering the medication
During:
Administer as indicated (right drug, right dosage, right frequency)
Clean the IV insertion for medication with a cotton ball with alcohol.
Gradually inject the drug into the port. Slow IV push to prevent
infiltration and phlebitis.
Administer cautiously and slowly with aseptic technique.
After:
Observe for the sensitivity and side effects to the drug
Reassess patients level of pain at least 15 and 30 minutes after
parenteral administration
Monitor circulatory and respiratory status and bladder and bowel
function.
Caution ambulatory patient about getting out of bed or walking.

X. HEALTH TEACHINGS
MEDICATION:
Folic Acid and Prednisone
EXERCISE:
Perform passive ROM exercise like flexion, extension of the extremities.
Brisk walking every morning.
TREATMENT:
Blood transfusion if blood count falls below normal.
Folic acid injection if available.
HEALTH TEACHING:
Encourage participation in recreation and regular exercise program
Provide appropriate level of environmental stimulation (e.i;music, TV/
radio, personal possessions and visitors)
Suggest use of sleep aid/ promote normal sleep/rest.
OPD:
Return to OPD for further check-up when there are changes on physical
strength.
DIET:
High fiber diet like vegetables and fruits.
Protein rich diet
Folic and vitamin B12 rich foods such as: liver, dried beans, peas,
wheat products, spinach, dark leafy vegetables, meat, eggs, milk
SIGNS/SYMPTOMS:
Observe for signs and symptoms such as body weakness, poor skin
turgor, pallor and weight loss