ANEMIA

DEFINITION

Anemia is a decrease in erythrocyte mass or amount of hemoglobin from

impaired production of erythrocytes, blood loss, or increased erythocyte
destruction. The pathophysiology, clinical manifestations, and selected
pathologies of anemia and their implications for nursing practice are
reviewed. As many as 4 million Americans have anemia; women younger
than age 65 have six times more anemia than men. Anemia is increasingly
a health problem for older adults, especially men over age 85 (Goddard,
McIntyre, & Scott, 2000). Anemia occurs when there is a decrease in red
blood cell numbers or a decrease in the amount of hemoglobin (Gaspad,
2005; Hodges, Rainey, Lappin, & Maxwell, 2007; Kumar, Cotran, &
Robbins, 2003). It is recognized most often when laboratory screening
tests are done because individuals often do not present with the signs and
symptoms of advanced anemia. Acute anemia usually is due to blood loss
or hemolysis (Adamson & Longo, 2001). Gastrointestinal bleeding or
bleeding from colon cancer can cause chronic blood loss that also
produces anemia (Goddard et al., 2000). In this article, the
pathophysiology of anemia, clinical manifestations, and selected diseases
that cause anemia will be reviewed, and the implications for nursing
practice discussed.

PATHOPHYSIOLOGY OF ANEMIA

All blood cells are produced by hematopoiesis in the bone marrow. The
major raw material essentials for this process are proteins, vitamin B12,
folic acid, and iron. Table 1 shows the substances needed for
hematopoiesis in this well-orchestrated cell function. Pathophysiology of
anemia differs according to its etiology. Acute or chronic red blood cell
loss, inadequate production of red blood cells in the bone marrow, or an
increased hemolysis can produce anemia (Gaspad, 2005; Hodges et al.,
2007). When anemia develops because of hemorrhage, the reduction in
red blood cell numbers causes a decrease in blood volume and the
cardiovascular (CV) system becomes hypovolemic. Anemia becomes
evident when the maximum level of hemodilution occurs, usually within 3
days after the acute blood loss. Hemodilution occurs in response to
decreased blood volume when fluid moves from the interstitium into the
intravascular space to expand the plasma volume. The decrease in blood
viscosity from the lower number of red blood cells, along with increased
intravascular fluid, causes the blood to flow faster through the CV system
and the flow becomes more turbulent. This process causes pressure on
the ventricles, the heart dilates, and heart valve dysfunction develops
(Metivier, Marchais, Guerin, Pannier, & London, 2000).

Hypoxia contributes to the changes in the CV and respiratory systems in

anemia by causing the blood vessels to dilate and the heart to contract
more forcefully, which further increases the demand for oxygen. Tissue
hypoxia causes the rate and depth of breathing to increase. Hemoglobin,
the oxygen-carrying protein in the red blood cells (RBCs), releases that
oxygen to the tissues more rapidly. When anemia becomes severe, the
body directs blood to the vital organs, such as the heart and the brain,
and renal blood flow decreases. Decreased renal blood flow in turn causes
an activation of the renin-angiotensin system response, leading to salt and
water retention. This process increases blood volume to improve kidney
function without changing tissue hypoxia in other organs (Gaspad, 2005;
Metivier et al., 2000).

Hemolytic Anemia

The pathophysiology of hemolytic anemia involves the destruction of

erthythrocytes and the subsequent acceleration of erythropoesis.
Hemolytic anemia may be inherited or acquired. The inherited form occurs
from cellular abnormalities in the membrane or the enzymes that
influence the production of hemoglobin. Acquired hemolytic anemia
occurs as a result of infection, chemical agents, and abnormal immune
response. Hemolytic anemia produces hemolyis within the blood vessels
or lymphoid tissue that filters blood. Immunohemolytic anemias are
caused by extravascular hemolysis and associated with autoimmune
mechanisms or drug reactions (Hodges et al., 2007; Mansen & McCance,
2006).

CLASSIFICATION OF ANEMIA

Classification by Morphology

Anemia can be classified by cell morphology or by etiology. Morphology,

the most common classification, includes cell size (cystic), color (chromic),
and shape of the RBCs. Measurements of hemoglobin, hematocrit, and red
cell indices provide information about the appearance of the RBC, which
aids in the classification. Red cell indices include the mean corpuscular
volume, mean hemoglobin, mean corpuscular hemoglobin concentration
(MCHC), and red blood cell distribution width (Hoekelman, Adam, Nelson,
Weitzman, & Wilson, 2001). In addition, serum ferritin concentration is
used to measure iron storage. Measuring ferritin concentration is
important in obtaining the diagnosis of iron deficiency anemia. Another
test, transferrin saturation, measures dietary iron absorption and
transport. Transferrin is the protein to which iron is bound for transport
from within the body (Lemone & Burke, 2004; Rote & McCance, 2008;
Uphold & Graham, 2003).

Classification by Etiology

Anemia can be caused by impaired cell production, blood loss, and

increased rate of destruction of the red cell. Blood loss occurs during
acute conditions such as trauma, or chronic diseases and gastrointestinal
bleeding. Increased rate of destruction of red cells occurs in hemolytic
anemia resulting from conditions inside and outside the cell. Abnormalities
within the red cell can result from hereditary or acquired disease.
Sperocytosis and elliptocytosis are hereditary conditions causing anemia
due to a disorder in the red cell membrane. Disorders in enzymes within
the red cell, such as glucose-6-phosphate dehydrogenase and pyruvate
synthesis diseases, also can cause anemia. Sickle cell anemia and
thalessemia are genetically determined diseases in which RBCs have
structural abnormalities (Kumar et. al., 2003).

Conditions existing outside the RBC include diseases of red cell

destruction, such as blood transfusion reactions, hemolytic anemia,
thrombocytopenia purpura, or disseminating intravascular coagulation.
Cell production can become impaired when there is a disturbance in
maturation and proliferation of red cells. Conditions in this category
include reduced erythropoietin, aplastic anemia, bone marrow
dysfunction, anemia from renal cell aplasia, and anemia from renal failure
or endocrine disorders. Impaired cell production occurs when cells have
defective DNA synthesis, such as in vitamin B12 and folic acid anemia.
Defective hemoglobin synthesis is the pathologic process for iron
deficiency anemia, thalessemia, and the anemia of chronic infections (Brill
& Baumgardner, 2000; Kumar et al., 2003).

SELECTED DISEASES CAUSING ANEMIA

Macrocytic Anemias

Macrocytic anemia occurs when the bone marrow produces very large
cells called macrocytes. These cells are large in size, thickness, and
volume. In addition to being larger, they also have an altered pattern of
chromatin deposits in the nucleus which helps distinguish them from
normocytes. Hemoglobin increases in proportion to the size of the cell.
The MCHC remains normal, producing normochromic cells (Dharmarajan,
Adiga, & Norkus, 2003; Mansen & McCance, 2006). The premature death
of these cells decreases their numbers in circulation, leading to the
manifestations of anemia (Rote & McCance, 2008).

In terms of the etiology of macrocytic anemias, both folic acid and vitamin
B12 are needed for normal hematopoiesis and maturation of all cells.
Hence, vitamin B12 deficiencies, folate deficiencies, inborn errors of
metabolism that inhibit folate absorption, and poor nutritional intake can
cause malabsorption syndromes leading to macrocytic anemia
(Dharmarajan et al., 2003; Hoekelman et al., 2001).

Pernicious anemia (vitamin B12 deficiency). Pernicious anemia is caused

by vitamin B12 deficiency. The term pernicious (highly destructive)
indicates the significant damage the disease produces and is a reminder
that it most often was fatal in the past. Pernicious anemia occurs in 20%-
30% of relatives of people with pernicious anemia. The disease usually is
seen in individuals over age 30, but older adults also are at risk (Suzuki et
al., 2004). Pernicious anemia develops when there is a lack of the intrinsic
factor enzyme that is required for absorption of vitamin B12. Intrinsic
factor and vitamin B12 complex are absorbed from the distal small
intestines. Pernicious anemia can occur following surgical removal of parts
of the stomach, or with gastric atrophy from chronic gastritis that causes
decreased secretion of intrinsic factor. Autoimmune conditions, which are
common in elders, also can produce pernicious anemia due to the
production of antibodies against gastric parietal cells (Dharmarajan et al.,
2003; Uphold & Graham, 2003).

Clinical manifestations of pernicious anemia are a result of the

inflammation of the gastric submucosa and subsequent degeneration of
parietal cells. The greater the loss of cells from the gastrointestinal tract,
the greater will be the lack of vitamin B12. Pernicious anemia develops
slowly over 20-30 years. Vague symptoms in the early stages of the
disease include infections, mood swings, and gastrointestinal and kidney
disease. The individual also may develop weakness and fatigue,
parasthesias of feet and fingers, and difficulty walking when the anemia
becomes severe. Damage to the posterior and lateral columns of the
spinal cord cause neurologic symptoms, such as loss of position, loss of
vibration sense, ataxia, spasticity, memory loss, and loss of appetite.
Gastrointestinal symptoms in later stages of the disease include
abdominal pain and a beefy red tongue. Individuals with pernicious
anemia have yellow, pale skin and an enlarged liver that ultimately
produces right-side heart failure. Their hemoglobin may be as low as 7 or
8 g/dL (Dharmarajan et al., 2003; Mansen & McCance, 2006; Uphold &
Graham, 2003). Folate deficiency. Folate (folic acid) is a vitamin required
for red cell production and maturation. Pregnant or lactating women
require a higher folate level for possible prevention of neural tube defects
in the fetus. Women capable of becoming pregnant should consume 400
ug from supplements or fortified foods. Folate is absorbed from the upper
intestine and is stored in the liver. Alcoholism, dietary fads, and a
lowvegetable diet can be precursors for folate deficiency. As may as 10%
of Americans have folate deficiency (Fink, 2004; Uphold & Graham, 2003).

Clinical manifestations of folate deficiency are similar to pernicious

anemia because malnourishment and anemia are the effects of this
disease. Individuals with folate deficiency have stomatitis and ulcerations
on the tongue. They may have dysphagia, flatulence, and watery diarrhea.
The neurologic changes that are present with pernicious anemia are not
evident with folate deficiency unless other vitamin deficiencies also exist
in the diet (Gaspad, 2005; Mansen & McCance, 2006).

Microcytic Anemias

In microcytic hypochromic anemia, red cells are small and have a reduced
amount of hemoglobin. Iron metabolism is essential for the development
of the red cell.
Iron deficiency anemia, thalassemia, and sideroblastic anemia present
with microcytic, hemochromic cells (Mansen & McCance, 2006; Uphold &
Graham, 2003). Iron deficiency anemia. As the most common type of
anemia in practice, iron deficiency occurs in 2%-5% of adult men and
postmenopausal women. Most cases of iron deficiency anemia in adults
result from failure to recapture iron in RBCs for hemoglobin synthesis (for
example, chronic blood loss from gastrointestinal bleeding or colon
cancer). Each milliliter of blood contains 0.5 mg of iron. Loss of 500
milliliters of blood creates a loss of 250 milliliters of iron, the equivalent of
25% of the body?s iron reserves. In iron deficiency anemia, the demands
for iron may exceed iron intake. This occurs in rapid growth periods, such
as pregnancy and adolescence, or during nutritional deprivation that may
occur in older adults. Blood loss of 10-20 milliliters of red cells per day is
greater than the amount of iron a person can absorb in the diet (Adamson
& Longo, 2001).

Any increase in the demand for iron or decrease in iron intake can cause
iron deficiency anemia. Clinical manifestations of iron deficiency anemia
include fatigue, pallor, fissures at the corners of the mouth, spooning of
fingernails, and reduced exercise tolerance. Diagnosis of iron deficiency
anemia depends on laboratory evidence. Anemia is defined as hemoglobin
less than 13 g/dL for men and less than 12 g/dL for women on at least one
laboratory assessment (Ioannou, Spector, Scott, & Rockey, 2002).

Thalassemias and sideroblastic anemia. The thalassemias are a group of

disorders caused by an imbalance between the beta-chain and alpha-
chain of the hemoglobin molecule. When one beta-chain is reduced, a
mild form of anemia called beta-thalassemia occurs. Defects in both beta-
chains result in a severe anemia called thalassemia major or Cooley?s
anemia. The clinical features of maxillary hyperplasia and prominence of
the frontal bones of the face occur in this type of anemia. This expansion
of the marrow of the facial bones and skull produces facial overgrowth
known as bossing. Alpha thalassemia is caused by a defect in two of the
alpha genes and produces a mild anemia similar to beta-thalassemia.
Thalassemia is found most often in Black, Mediterranean, and Southeast
Asian ethnic groups (Segal, 2004).

Sideroblastic anemia is either acquired or hereditary. The acquired form is

most common; it usually has no known etiology but may be associated
with other conditions, such as alcoholism, drug reactions, copper
deficiency, or hypothermia. Hereditary sources of sideroblastic anemia
that occur from an X-linked transmission pattern only affect males.
Females have hereditary sideroblastic anemia from autosomal
transmission. Sideroblastic anemia may be present in childhood but it is
most common is midlife (Mansen & McCance, 2006).

Clinical manifestations of sideroblastic leukemia are similar to other

anemias, but affected individuals also have signs of iron overload.
Enlargement of the spleen and liver occur. Individuals with sideroblastic
anemia occasionally have a bronze-colored skin tone. Neurologic
impairment does not occur in this type of anemia, but the
cardiopulmonary systems are taxed from heart rhythm disturbance and
congestive heart failure (Mansen & McCance, 2006).

Normocytic Anemias

Normocytic anemias are characterized by cells of normal size with normal

hemoglobin content. The anemia occurs because the number of red cells
is low. Normocytic anemias are less common than macrocytic or
microcytic anemia. Several diseases result in normocytic anemia,
including aplastic anemia, acute blood loss, hemolytic anemia, and
anemia of chronic disease (Gaspad, 2005; Young, Calado, & Scheinberg,
2006).

Aplastic anemia. Aplastic anemia, also known as hypoplastic anemia,

produces a decline in blood cell production due to bone marrow
depression. Panocytopenia also may occur in this type of anemia, resulting
in the absence of all three types of blood cells. The rate of decline in the
bone marrow production of blood cells is slower for red cells than other
types of cells, so the appearance of this anemia in adults is similar to a
chronic anemia pattern. Aplastic anemia occurs rarely, but it is increasing
in developing countries. Aplastic anemia can be either hereditary or
acquired after birth. The most common hereditary form of aplastic anemia
is called Fanconi anemia. It results from defects in DNA repair. Acquired
aplastic anemia also occurs secondary to another disease, such as
reactions to benzene, arsenic, chloramphenicol (Chloromycetin?),
phenytoin (Dilantin ?), and antimetabolite chemotherapeutic drugs (6-
mercaptopurine, vincristine, and busulfan). Ionizing radiation can cause
secondary aplastic anemia (Gaspad, 2005; Young et al., 2006).

The clinical manifestations of aplastic anemia may develop slowly

depending on which cells in the bone marrow are damaged and how fast
the damage occurs. If there is a rapid onset of aplastic anemia, clinical
manifestations include hypoxia, pallor, weakness, fever, and dyspnea. The
slower progression of the disease produces clinical manifestations of
progressive weakness, susceptibility to infection, low-grade fever, cellulitis
in the neck, and ulceration and hemorrhaging in the nose, mouth, and
gastrointestinal tract. The individual may develop waxy and pale skin
tones. An individual with aplastic anemia has an extremely low
hemoglobin of approximately 7 g/ dL. White cell and platelet numbers will
be low due to alterations of manufacturing and production in the bone
marrow (Gaspad, 2005; Young et al., 2006).

Acute blood loss. Acute blood loss can result in normocytic, normochromic
red cell appearance. As much as 1,500 to 2,000 milliliters of blood can be
lost without causing symptoms when the individual is prone, but light
headedness is experienced when standing. Chronic bleeding produces
fewer, less intense symptoms. Acute and chronic blood loss are treated by
restoring blood volume with saline, dextran, albumin, or plasma (Adamson
& Longo, 2001; Mansen & McCance, 2006).

Hemolytic anemias.Warm antibody hemolytic anemia is the most common

type of immunohemolytic anemia and affects females over age 40. The
mediating antibody for this process is immunoglobulin that attacks the
RBCs. Warm antibody hemolytic anemia usually is idiopathic but also may
be due to other conditions, such as lymphomas, leukemias, and other
neoplastic disorders in about 50% of affected individuals. Other conditions
associated with warm antibody hemolytic anemia are systemic lupus
erythematosis or exposure to one or more drugs, such as a- Methyldopa
(Aldomet?), penicillin (Bicillin?), and quinidine (Novoquinidin ?) (Adamson
& Longo, 2001; Gaspad, 2005).

Cold agglutin immune hemolytic anemia is a less common condition

mediated by immunoglobulin. This type of anemia occurs in cooler
temperatures, with clinical manifestations similar to Raynaud?s disease.
Cold agglutin anemia results from vascular obstruction rather than
hemolysis. Diseases associated with development of cold agglutin anemia
are mycoplasma pneumonia, lymphoid malignancies, Epstein Barr virus,
cytomegalovirus infection, mumps, and Legionnaires disease (Mansen &
McCance, 2006). Cold hemolysis hemolytic anemia is a rare disorder that
causes massive hemolyis after exposure to cold temperatures. It is
associated with several diseases, such as mycoplasma pneumonia,
measles, mumps, nonspecific flu, and other viral syndromes. Syphilis
causes a chronic type of this disease (Mansen & McCance, 2006).

The clinical manifestations of hemolytic anemia vary widely. The severe

form of the disease usually is diagnosed at birth or within the first year of
life. Mild-tomoderate disease is more common. There may be no
symptoms unless there are other complications. Jaundice is a frequent
symptom. An aplastic crisis can occur when the bone marrow and cell
production fail. Papavirus B19 infection is a common cause of aplastic
crisis and splenomegaly frequently occurs because the spleen becomes
markedly enlarged from the breakdown of cells. Enlarged spleens become
fragile and vulnerable to trauma (Gaspad, 2005; Mansen & McCance,
2006). Anemia of chronic illness. Anemia can occur when individuals have
a chronic disease, though the cause is uncertain (Uphold & Graham,
2003). Chronic anemia usually is mild to moderate. Diseases that produce
a chronic form of anemia include acquired immunodeficiency disease,
chronic inflammatory bowel conditions, chronic renal failure, rheumatoid
arthritis, systemic lupus erythematosus, acute and chronic hepatitis, and
malignancies. This type of anemia develops 1-2 months after the
beginning of the chronic disease. It produces normocytic and
normochromatic red cells, but they also may be microcytic and
hypochromic if the chronic disease produces iron deficiency (Thomas,
2004; Uphold & Graham, 2003).
The anemia of chronic illness produces a red cell with a decreased life
span. In addition, the bone marrow does not respond by increasing red cell
production. Altered iron metabolism also is possible. Impaired iron
metabolism is impacted by lactoferrin and apoferrritin, which are present
in the blood in small amounts. When infection or inflammation is present,
neutrophils release lactoferrin or apoferritin. When iron binds to lactoferrin
and apoferritin, it is converted to intoferritin and stored rather than being
available for hemoglobin development (Gaspad, 2005).

Anemia of chronic illness is mild and only may impact physical activity
unless the decrease in hemoglobin is significant. The treatment for this
form of anemia is to address the iron deficiency and eliminate the primary
disorder. If there is no infection or inflammation but anemia is present, a
malignancy should be suspected (Gaspad, 2005; Thomas, 2004).

IMPLICATIONS FOR NURSING CARE

Assessment

The nursing assessment of the patient with a potential for anemia

includes both subjective and objective data. The nurse should review the
patient?s medical history to determine the occurrence of recent blood loss
or trauma, chronic liver disease, endocrine or renal disease,
gastrointestinal bleeding, malabsorption syndrome, ulcers, gastritis or
hemorrhoids, and surgery or radiation therapy. Inflammatory disorders
such as Crohn?s disease and exposure to radiation, arsenic, lead,
benzenes, and copper should be investigated (Jones, 2004). The patient?s
medications should be identified, including iron supplementations, aspirin,
anticoagulants, oral contraceptives, phenobaribital (Luminal ?),
nonsteroidal anti-inflammatory drugs, quinine, phenytoin, a- Methyldopa,
penicillin and quinidine (Adamson & Longo, 2001; Broyles, Reiss, & Evans,
2007; Jones, 2004; Smeltzer, Bare, Hinkle, & Cheever, 2008).

Clinical manifestations of anemia are not evident until the patient?s

hemoglobin is less than 6-7 g/dL. The patients with higher hemoglobin
may have only palpitations and dyspnea on exertion as clinical
manifestation of anemia. With severe anemia, the patient may have
lymphadenopathy and fever. Table 2 shows the symptoms associated with
hemoglobin below 6-7 g/dL (Jones, 2004; Smeltzer et al., 2008).

The patient with anemia will have a low red blood cell count, hemoglobin,
and hematocrit. The serum iron may be low. Ferritin, folate, and serum
erythropoietin may be altered. Other laboratory data that may be altered
in anemia are the bilirubin, platelet count, and total serum binding
capacity. Anemia sometimes is caused by destruction of RBCs producing
an elevated bilirubin. High serum bilirubin can injure the lipid components
of the plasma membrane. In addition, because plasma proteins bind to
unconjugated bilirubin, high serum counts also can lead to structural
injury to the cells due to the loss of cellular proteins (Rote, McCance, &
Manson, 2008; Smeltzer et al., 2008). Patient history and laboratory data
often point clearly to the etiology for the anemia as a process of RBC
destruction or inadequate production (Smeltzer et al., 2008).
Understanding laboratory examination of cell morphology is helpful in
planning care for the patient and educating patient and family regarding
symptoms of anemia (Jones, 2004).

Intervention

Nursing interventions depend on the etiology of the anemia. The major

nursing diagnoses applicable to many patients with anemia include
activity intolerance related to weakness, fatigue, and general malaise;
altered nutrition, less than body requirements, related to inadequate
intake of essential nutrients; altered tissue perfusion related to
inadequate blood volume or hematocrit; and noncompliance with
prescribed therapy. Blood or blood products may be ordered if acute blood
loss is the reason for the anemia. The nurse also should monitor vital
signs and oxygen saturation. When hemoglobin is low, the heart
compensates by increasing the workload, producing initial symptoms of
tachycardia, palpitations, and dyspnea. Long-term effects would include
cardiomegaly and hepatomegaly (Jones, 2004; Lemone & Burke, 2004;
Smeltzer et al., 2008). Monitoring laboratory results will direct the nurse in
understanding the etiology for the anemia. Fatigue is a distressing
symptom for most individuals with anemia. Nursing interventions should
be directed at establishing balance between activities in the day, planning
rest periods, and establishing a physical activity program (Smeltzer et al.,
2008).

If the patient has iron deficiency anemia or other anemia with dietary
etiology, dietary education and lifestyle changes will be needed. Financial
planning may be needed if poverty or sudden loss of family income is
contributing to a low iron intake or other dietary deficiency. The patient
and family should be involved in planning for dietary changes. Small
frequent meals during the day may increase the patient?s ability to
maintain a nutritious diet, especially if the patient is an older adult or
living alone (Jones, 2004; Lemone & Burke, 2004).

The nurse should educate the patient about how to take iron supplements
and additional vitamins. Iron is absorbed from the duodenum and proximal
jejunum. Iron preparations are enteric coated and given three times a day,
or once a day using a higher dose. Iron is best absorbed as ferrous sulfate
in an acid environment, and it should be given about an hour before
meals. Taking vitamin C with iron helps absorption. Because iron can stain
teeth, elixirs should be diluted and ingested through a straw. Iron causes
gastrointestinal side effects, such as heartburn, constipation, and
diarrhea. To decrease these effects, the dose of iron may be reduced or
ferrous gluconate may be used as a substitute. Parenteral iron is given
when the anemia is severe and cannot be managed adequately by diet
changes or medication. Iron-dextran is the most common parenteral form
used in the United States (Jones, 2004; Smeltzer et al., 2008). The nurse
should evaluate the patient?s understanding of dietary issues contributing
to the anemia. A 24-hour food log will assist the nurse to evaluate the
intake of protein, iron, calories, and other nutrients needed for
hematopoiesis.

The nurse should monitor the patient for the expected outcomes of
nursing interventions. Does the patient tolerate activities and follow a
program of progressive activities and rest? Does he or she maintain an
adequate, well-balanced diet and comply with the nutritional supplements
suggested through the treatment plan? Ongoing monitoring of the
patient?s laboratory data will determine the status of the anemia.
Monitoring the vital signs at rest and during activity will demonstrate the
patient?s activities of daily living (Lemone & Burke, 2004). Are the vital
signs within the patient?s baseline? Are pulse oximetry readings (oxygen
saturation) values within normal limits (Lemone & Burke, 2004; Smeltzer
et al., 2008)? Is the patient free of complications from the anemia? Do the
patient and family verbalize understanding of the rationale for the
treatment program (Smeltzer et al., 2008)? Evaluation of the outcome of
teaching and therapy will depend on the etiology of the anemia and
treatment plan (Jones, 2004). The patient and family often are anxious
and may need additional literature in the language of their choice to
support the education component of the nurse?s role.

Summary and Conclusions

The nurse should be aware of the pathophysiology and etiology of anemia.

Careful assessment and ongoing monitoring are essential, especially when
anemia results from acute blood loss. Ongoing monitoring of laboratory
data and physical signs of cardiovascular health will be necessary until the
patient demonstrates vital signs within his or her baseline and pulse
oximetry results within normal limits (Smeltzer et al., 2008). The nurse
consistently monitors the patient?s tolerance for daily activities and the
dietary intake and nutritional status. The nurse is responsible for
educating the patient and family about the cause of anemia as well as
diet and medications required to address a low hemoglobin and
hematocrit. The patient and family should be involved in determining the
necessary lifestyles changes (Jones, 2004). Understanding of the disease
process of the anemia and assisting the patient and family to manage the
treatment plan are valuable contributions the nurse can make to the
patient.
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