ANEMIA

Anemia is a deficiency in the number of

erythrocytes(RBCs), the quantity and quality
of hemoglobin, and or the volume of packed
RBCs.
 Definition
Anemia is a clinical condition that results
from an insufficient supply of healthy red
blood cells (RBCs), the volume of packed
RBCs, and or the quantity of hemoglobin.
Hypoxia results because the body’s tissues are
not adequately oxygenated.
 Causes of anemia
Decreased RBC production
– Deficient nutrients
• Iron
• Cobalamin
• Folic acid
• Decreased erythropoietin
• Decreased iron availability
Blood loss
– Chronic hemorrhage
• Bleeding duodenal ulcer
• Colorectal cancer
• Liver disease
• Acute trauma
• Ruptured aortic aneurysm
• GI bleeding
Increased RBC destruction
– Hemolysis
• Sickle cell disease
• Medication (eg. Methyl dopa)
• Incompatible blood
• Trauma(cardiopulmonary bypass)
 Classification of anemia

• Decreased RBC Production

Decreased Hemoglobin Synthesis
– Iron deficiency
– Thalassemias (decreased globin synthesis)
– Sideroblastic anemia (decreased porphyrin)
 Defective DNA Synthesis
• Cobalamin (vitamin B12) deficiency
• Folic acid deficiency
 Decreased Number of RBC Precursors
• Aplastic anemia and inherited disorders (e.g.,
Fanconi syndrome)
• Anemia of myeloproliferative diseases (e.g.,
leukemia) and myelodysplasia
• Chronic diseases or disorders
• Medications and chemicals (e.g.,
chemotherapy, lead)
• Radiation
• Blood Loss
Acute
• Trauma
• Blood vessel rupture
• Splenic sequestration crisis
 Chronic
• Gastritis
• Menstrual flow
• Hemorrhoids
• Increased RBC Destruction (Hemolytic
Anemias)
Hereditary (Intrinsic)
• Abnormal hemoglobin (sickle cell disease)
• Enzyme deficiency (G6PD)
• Membrane abnormalities (paroxysmal
nocturnal hemoglobinuria, hereditary
spherocytosis)
• Acquired (Extrinsic)
• Macroangiopathic: physical trauma
(prosthetic heart valves. extracorporeal
circulation)
• Microangiopathic: disseminated
intravascular coagulopathy (DIC). thrombotic
thrombocytopenic purpura (TTP)
• Antibodies (isoimmune and autoimmune)
• Infectious agents (e.g.. malaria) and toxins
 Pathophysiology
• Transport of oxygen is impaired with anemia.
• Hemoglobin is lacking or the number of RBCs is too
low to carry adequate oxygen to tissues and hypoxia
develops.
• The body attempts to compensate for tissue hypoxia
by increasing the rate of RBC production, increasing
cardiac output by increasing stroke volume or heart
rate, and shifting the oxygen-hemoglobin dissociation
curve to the right to facilitate the removal of more
oxygen by the tissues at the same partial pressure of
oxygen.
 Clinical Manifestations
• Specific manifestations vary depending on the
rate at which the anemia has evolved, its
severity, and any coexisting disease.
• Hemoglobin (Hgb) levels are often used to
determine the severity of anemia.
• Mild states of anemia (Hgb 10 to 12 g/dL
[100 to 120 g/L]) may exist without causing
symptoms.
• In moderate anemia (Hgb 6 to 10 g/dL [60
to 100 g/L]) the cardiopulmonary symptoms
are increased.
• In severe anemia (Hgb less than 6 g/dL [60
g/L]) the patient has many clinical
manifestations involving multiple body
systems.
• Integumentary Changes.
• Integumentary changes include pallor,
jaundice, and pruritus.
• The skin, the sclera of the eyes and mucous
membranes should be evaluated for jaundice
because they reflect the integumentary
changes more accurately, especially in a dark-
skinned individual.
 Cardiopulmonary Manifestations.
• Cardiac output is maintained by increasing the
heart rate and stroke volume.
• The low viscosity of the blood contributes to
the development of systolic murmurs and
bruits.
• Heart failure (HF), cardiomegaly, pulmonary
and systemic congestion, ascites, and
peripheral edema may develop if the heart is
overworked for an extended period.
 Medical Management
• The goals of care for clients with anemia
include
(1) alleviating or controlling the causes
(2) relieving the manifestations
(3) preventing complications.
 Alleviate and Control the Causes
• Depending on the etiology of the anemia,
interventions may include
(1) supplemental iron therapy,
(2) nutritional therapy,
(3) surgery to repair sites of hemorrhage,
(4) splenectomy,
(5) removal of toxic agents that cause aplasia,
(6) stem cell or bone marrow transplantation,
(7) corticosteroid therapy, and
(8) immunosuppressive therapy.
 Relieve Manifestations
• Oxygen Therapy.
• Oxygen therapy may be prescribed for clients
with severe anemia.
• Oxygen helps to prevent tissue hypoxia and
lessens the workload of the heart as it struggles
to compensate for the lower Hb levels.
 Erythropoietin.
• Subcutaneous injections of erythropoietin can
be given to treat anemias of chronic disease
because this drug increases the production of
RBCs.
 Iron Replacement.
• Iron can be given to augment oral intake in
cases where the need for iron is immediate or
the demands are beyond dietary measures
(e.g., pregnancy).
• The oral form of iron should be used because
it is inexpensive and convenient. It is usually
given for mild forms of anemia.
• The medications of choice are ferrous sulfate
(Feosol) or ferrous gluconate (Fergon), 200 to
325 mg orally in three or four doses a day, with
or after meals.
• Taking iron with vitamin C or orange juice aids
in the absorption of iron.
• Clients usually receive iron supplements for at
least 6 months for repletion of the body stores.
• Side effects may include nausea, vomiting,
constipation or diarrhea, and blackened stools.
 Blood Component Therapy
• Blood products obtained from another person are
called homologous. Those reinfused from the
client's own blood are called autologous.
• Transfusion Reactions Associated with
Homologous Blood Transfusions.
• A blood transfusion reaction is an adverse reaction
to blood component therapy that can range from
mild symptoms to a life-threatening condition.
• Complications can be acute or delayed, occurring
days to years after a transfusion.
• Acute reactions may be immunogenic or non
immunogenic. Immunogenic reactions include
allergic, acute hemolytic, and anaphylactic
reactions as well as fever; non immunogenic
reactions include circulatory overload and
septicemia.
• Delayed reactions may include a delayed
hemolytic reaction, hepatitis B, hepatitis C,
HIV, GVHD (graft vs host ), iron over load,
and other infections and agents such as CMV,
EBV, human T-cell leukemia virus type 1
(HTLV-1(human t lymphotropic virus), the
organism that causes malaria), and West Nile
virus.
• Autologous Blood Transfusion.
• Autologous blood transfusion is the alternative
to homologous (random) transfusion .
• Clients who do not have leukemia or
bacteremia should be offered the option of
donating their own blood before a scheduled
surgical procedure when there is a reasonable
expectation that blood will be required.
• Autologous donations can be made every 3
days if the donor's Hb level remains at or
above 11 g/dl.
• For the blood to be maintained in a liquid
state, donations should begin within 5 weeks
of the transfusion date. Donations should cease
at least 3 days before the date of transfusion.
 ANEMIA CAUSED BY DECREASED
ERYTHROCYTE PRODUCTION 
• The normal life span of an RBC is 120 days.
• Three alterations in erythropoiesis may occur
that decrease RBC production:
(1) decreased hemoglobin synthesis may lead
to iron-deficiency anemia, thalassemia, and
sideroblastic anemia;
 (2) Defective deoxyribonucleic acid (DNA)
synthesis in RBCs (e.g., cobalamin deficiency,
folic acid deficiency) may lead to
megaloblastic anemias; and
(3) Diminished availability of erythrocyte
precursors may result in aplastic anemia and
anemia of chronic disease.
 Iron-deficiency anemia
• Iron-deficiency anemia, one of the most
common chronic hematologic disorders, is
found in 2% to 5% of adult men and post
menopausal women in developed countries.
• In India, the prevalence of anemia is 70% to
80% in children, 70% in pregnant women, and
24% in men.
 Definition
Iron deficiency anemia is a chronic ,
hypochromic microcytic anemia resulting from
an insufficient supply of iron in the body.
Without iron , hemoglobin concenteration in
the RBCs is reduced and the cells are unable to
oxygenate the body’s tissues adequately,
resulting in anemia.
 Etiology
• Normal dietary iron intake is usually sufficient to meet
the needs of men and older women, but it may be
inadequate for those individuals who have higher iron
needs (e.g., menstruating or pregnant women).
• Malabsorption of iron may occur after certain types of
gastrointestinal (GI) surgery and in malabsorption
syndromes.
• As iron absorption occurs in the duodenum,
malabsorption syndromes may involve disease of the
duodenum in which the absorption surface is altered or
destroyed.
• Blood loss is a major cause of iron deficiency
in adults. Two milliliters of whole blood contain
1 mg of iron. The major sources of chronic
blood loss are from the GI and genitourinary
(GU) systems.
– Loss of 50 to 75 mL of blood from the upper GI
tract is required for stools to appear black (melena).
The black color results from the iron in the RBCs.
– Common causes of GI blood loss are peptic ulcer,
gastritis, esophagitis, diverticuli, hemorrhoids, and
neoplasia.
– Genito urinary blood loss occurs primarily from
menstrual bleeding. The average monthly
menstrual blood loss is about 45 mL and causes
the loss of about 22 mg of iron.
– Postmenopausal bleeding can contribute to anemia
in a susceptible older woman.
– In addition to anemia of chronic kidney disease,
dialysis treatment may induce iron-deficiency
anemia because of the blood lost in the dialysis
equipment and frequent blood sampling.
 Pathophysiology
• Iron is present in all RBCs as heme in Hb;
heme accounts for two thirds of the body's iron.
• Iron is also vital for the metabolic processes of
DNA synthesis and electron transport.
• Iron concentration in the body is regulated by
the absorptive cells in the proximal small
intestine; these cells alter iron absorption to
match body losses of iron intake. Errors in this
balance also lead to anemia.
• Fortunately the GI tract can increase its
absorption of iron from 10% daily to about
20% to 30% daily.
• In this way, the body often compensates for
diminishing iron stores resulting from
inadequate iron intake or excessive iron loss.
• The other one third of the body's iron (non-
heme) is stored in the form of ferritin, an iron-
phosphorus-protein complex that contains
about 23% iron.
 Clinical Manifestations
• Pallor is the most common finding, and
glossitis (inflammation of the tongue) is the
second most common. Another finding is
cheilitis (inflammation of the lips).
• The patient may report headache, paresthesias,
and a burning sensation of the tongue, all of
which are caused by lack of iron in the tissues.
 Diagnostic Studies

• History and physical examination

• Hct and hb levels
• RBC count including morphology
• Reticulocyte count
• Serum iron
• Serum ferritin
• Serum transferrin
• Total iron binding capacity
• Other diagnostic studies (e.g., stool guaiac test)
are done to determine the cause of the iron
deficiency.
• Endoscopy and colonoscopy may be used to
detect GI bleeding.
• A bone marrow biopsy may be done if other
tests are inconclusive.
 Collaborative Care
• The main goal is to treat the underlying disease
that is causing reduced intake (e.g., malnutrition,
alcoholism) or absorption of iron.
• Teach the patient which foods are good sources of
iron.
• If nutrition is already adequate, increasing iron
intake by dietary means may not be practical.
• If the iron deficiency is from acute blood loss, the
patient may require a transfusion of packed RBCs.
 Drug Therapy.

1. Iron is absorbed best from the duodenum

and proximal jejunum. Therefore enteric-
coated or sustained-release capsules, which
release iron farther down in the Gl tract, are
counterproductive and expensive.
 2. The daily dose should provide 150 to 200
mg of elemental iron. This can be ingested in
three or four daily doses, with each tablet or
capsule of the iron preparation containing
between 50 and 100 mg of iron (e.g., a 300-mg
tablet of ferrous sulfate contains 60 mg of
elemental iron).
 3. Iron is best absorbed as ferrous sulfate (Fe²)
in an acidic environment. For this reason and
to avoid binding the iron with food, iron
should be taken about an hour before meals,
when the duodenal mucosa is most acidic.
Taking iron with vitamin C (ascorbic acid) or
orange juice, which contains ascorbic acid,
enhances iron absorption. Gastric side effects,
however, may necessitate ingesting iron with
meals.
4. Undiluted liquid iron may stain the patient's
teeth. Therefore it should be diluted and
ingested through a straw.
 5. GI side effects of iron administration may occur,
including heartburn, constipation, and diarrhea. If side
effects develop, the dose and type of iron supplement
may be adjusted. For example, many individuals who
need supplemental iron cannot tolerate ferrous sulfate
because of the effects of the sulfate base. However,
ferrous gluconate may be an acceptable substitute. Tell
patients that the use of iron preparations will cause their
stools to become black because the GI tract excretes
excess iron. Constipation is common, and the patient
should be started on stool softeners and laxatives, if
needed, when started on iron.
• In some situations it may be necessary to
administer iron parenterally. Parenteral use of
iron is indicated for malabsorption, intolerance
of oral iron, a need for iron beyond oral limits,
or poor patient adherence in taking the oral
preparations of iron.
• Parenteral iron can be given intramuscularly
(IM) or IV. An iron-dextran complex contains
50 mg/mL of elemental iron available in 2-mL
single-dose vials.
• Sodium ferrous gluconate and iron sucrose are
alternatives and may carry less risk of life-
threatening anaphylaxis.
• Because IM iron solutions may stain the skin,
separate needles should be used for
withdrawing the solution and for injecting the
medication. Use a Z-track injection technique.
 Medical Management
• Anemia may be a sign of a curable Gl cancer
or of uterine fibroid tumors Stool specimens
should be tested for occult blood.
• People 50 years of age or older should have
periodic colonoscopy, endoscopy.
• X-ray examination of the GI tract to detect
ulcerations, gastritis, polyps, or cancer.
• Several oral iron preparations-ferrous sulfate,
ferrous gluconate, and ferrous fumarate are
available for treating iron deficiency anemia.
• Iron store replenishment takes much longer, so
it is important that the patient continue taking
the iron for as long as 6 to 12 months.
• Vitamin C facilitates the absorption of iron.
• In some cases, oral iron is poorly absorbed or
poorly tolerated, or iron supplementation is
needed in large amounts. In these situations,
IV or intramuscular (IM) administration of
iron dextran may be needed.
• Before parenteral administration of a full dose,
a small test dose should be administered
parenterally to avoid the risk of anaphylaxis
with either IV or IM injections.
• Emergency medications (eg, epinephrine)
should be close at hand. If no signs of allergic
reaction have occurred after 30 minutes, the
remaining dose of iron may be administered.
Several doses are required to replenish the
patient's iron stores.
 Nursing Management
• Food sources high in iron include organ meats
(beef or calf's liver, chicken liver), other
meats, beans (black, pinto, and garbanzo),
leafy green vegetables, raisins, and mo lasses.
Taking iron-rich foods with a source of
vitamin C (eg, orange juice) enhances the
absorption of iron.
• Iron is best absorbed on an empty stomach, the
patient is instructed to take the supplement an hour
before meals.
• Iron supplements are usually given in the oral
form, typically as ferrous sulfate.
• Tablets with enteric coating may be poorly
absorbed and should be avoided.
• Many patients have difficulty tolerating iron
supplements because of GI side effects (primarily
constipation, but also cramping, nausea, and
vomiting).
• If taking iron on an empty stomach causes gastric
distress, the patient may need to take it with meals.
• Antacids or dairy products should not be taken
with iron, because they greatly diminish its
absorption.
• Liquid forms of iron that cause less GI distress are
available. However, they can stain the teeth; the
patient should be instructed to take this medication
through a straw, to rinse the mouth with water, and
to practice good oral hygiene.
 Thalassemia
Definition
• Thalassemia is an autosomal-recessive genetic
disorder that results in inadequate normal Hb
production. Whereas IDA affects heme
synthesis, thalassemia disrupts the synthesis of
globin.
• Those who inherit just one beta-gene
(heterozygotes) have thalassemia minor, also
called thalassemia trait, the carrier state of
thalassemia major.
• Those who inherit both beta-genes
(homozygotes) have thalassemia major,
which results in a profound and life-
threatening anemia.
• The alpha-thalassemias are milder than the
beta forms and often occur without symptoms;
the erythrocytes are extremely microcytic, but
the anemia, if present, is mild.
• The severity of beta-thalassemia varies
depending on the extent to which the
hemoglobin chains are affected.
• Patients with mild forms have a microcytosis
and mild anemia.
• Bone marrow transplant (BMT) offers a
chance of cure, but when this is not possible,
the disease is usually treated with transfusion
of PRBCS.
• Patients may survive into their 20s and 30s,
Patient teaching during the reproductive years
should include preconception counseling about
the risk of thalassemia major.
 Pathophysiology
• In alpha-thalassemia, there is a mutation in
the alpha-globin gene(s).
• In thalassemia minor, one beta-globin gene
is mutated, leading to minor disruptions in beta-
globin synthesis.
• In thalassemia major, a mutation exists in
both beta-genes, resulting in significant
impairment of beta-globin synthesis, marked
reduction in hemoglobin production, and
profound anemia.
• Hemolysis results from an imbalance in the
alpha- and beta-globin chains, which are
normally paired.
• The excess unpaired alpha or beta-globin
chains aggregate and form a precipitate that
damages RBC membranes, leading to
intravascular hemolysis.
 Thalassemia Major
• Thalassemia major (Cooley's anemia) is
characterized by severe anemia, marked hemolysis,
and ineffective erythropoiesis (production of
erythrocytes).
• Organ dysfunction due to iron overload results from
the excessive amounts of iron in multiple PRBC
transfusions.
• Regular chelation therapy (eg, subcutaneous
deferoxamine) has reduced the complications of iron
over load and prolonged the life of these patients.
 Clinical Manifestations
• The patient with thalassemia minor is frequently
asymptomatic. The patient has mild to moderate
anemia with microcytosis (small cells) and
hypochromia (pale cells).
• Thalassemia major is a life-threatening disease
in which growth, both physical and mental, is
often retarded.
• The person who has thalassemia major is pale
and displays other general symptoms of anemia.
• Jaundice from the hemolysis of RBCs is
prominent.
• The person has pronounced splenomegaly.
• Hepatomegaly and cardiomyopathy may
occur from iron deposition
• As the bone marrow responds to the reduced oxygen-
carrying capacity of the blood, RBC production is
stimulated and the marrow becomes packed with
immature erythroid precursors that die. This stimulates
further erythropoiesis, leading to chronic bone marrow
hyperplasia and expansion of the marrow space. This
may cause thickening of the cranium and maxillary
cavity.
• Cardiac complications from iron overload, pulmonary
disease, and hypertension also contribute to early death.
• Endocrinopathies (hypogonadotrophic hypogonadism)
and thrombosis also be complications of the disease.
• Thrombocytosis after spleen dysfunction
and/or removal may occur.
• Patients with thalassemia may have hepatitis C
because of having received blood transfusions
before donated blood was screened for
hepatitis C .
• Hepatitis C may result in cirrhosis and
hepatocellular carcinoma.
 Collaborative Care
• No specific drug or diet therapies are effective
in treating thalassemia.
• Thalassemia minor requires no treatment
because the body adapts to the reduction of
normal hemoglobin.
• Thalassemia major is managed with blood
transfusions or exchange transfusions in
conjunction with oral deferasirox, or
deferiprone or deferoxamine (chelating agents
that bind to iron) is given IV or
subcutaneously to reduce the iron overloading
(hemochromatosis) that occurs with chronic
transfusion therapy.
• Folic acid is given if there is evidence of
hemolysis.
• Transfusions are administered to keep the
hemoglobin level at approximately 10 g/dL
(100 g/L) to maintain the patient's own
erythropoiesis without causing the spleen to
enlarge.
• Zinc supplementation may be needed, since zinc
is reduced with chelation therapy.
• Ascorbic acid supplementation may be needed
during chelation therapy, since it increases urine
excretion of iron. Other than during chelation
therapy, ascorbic acid should not be taken because
it increases the absorption of dietary iron.
• Iron supplements should not be given.Because
RBCs are sequestered in the enlarged spleen,
thalassemia major may be treated by splenectomy.
• Hepatic, cardiac, and pulmonary organ
function should be monitored and treated as
appropriate.
• Although hematopoietic stem cell
transplantation (HSCT) remains the only cure
for patients with thalassemia, the risk of this
procedure may outweigh its benefits.
• With proper iron chelation therapy, patients are
living longer.
 Megaloblastic anemia
• Definition
• Megaloblastic anemias are a group of
disorders caused by impaired DNA synthesis
resulting in defective, large RBCS
(megaloblasts). They are caused by
deficiencies of vitamin B12 (cobalamin) and
folic acid.
• Cobalamin/B12 Deficiency (Pernicious
Anemia)
• Pernicious anemia is an autoimmune disorder
characterized by the absence of intrinsic factor
(IF) in gastric secretions, leading to
malabsorption of cobalamin (vita min B ₁2).
Pernicious anemia has been incorrectly used to
describe any cobalamin deficiency, but it is
actually only one cause of inadequate
cobalamin.
 Etiology and Risk Factors
• Pernicious anemia (PA) is the most prevalent form of
vitamin B12 deficiency in the United States and Canada.
• It is associated with gastric atrophy and loss of IF as well
as a rare genetic autosomal-recessive disorder (congenital
pernicious anemia) in which IF is lacking without gastric
atrophy.
• Ninety percent of people with PA have antibodies that react
specifically against the parietal gastric cells where IF is
produced; 60% have anti-IF antibodies.
• It occurs more often in families of PA clients and is
associated with human leukocyte antigen (HLA) types A2,
A3, and B7 and in type A blood groups.
• PA typically arises in people between 40 and
70 years of age with peak incidence around 70
years of age.
• It is more prevalent in people of Celtic and
Scandi navian ancestry.
 Classification of Megaloblastic Anemia
• Cobalamin (Vitamin B₁2) Deficiency Dietary
deficiency
– Deficiency of gastric intrinsic factor
– Pernicious anemia
– Gastrectomy
– Intestinal malabsorption
– Increased requirement
– Chronic alcoholism
• Folic Acid Deficiency
• Dietary deficiency (e.g., leafy green vegetables,
citrus fruits)
• Malabsorption syndromes
• Drugs interfering with absorption or use of folic acid
• Methotrexate
• Antiseizure drugs (e.g., phenobarbital, phenytoin )
• Increased requirement
• Alcohol abuse
• Anorexia
• Hemodialysis patients (folic acid lost during dialysis)
• Drug-Induced Suppression of DNA
Synthesis
– Folate antagonists
– Metabolic inhibitors.
– Alkylating agents
 Inborn Errors
• Defective folate metabolism
• Defective transport of cobalamin
 Clinical Manifestations
• The major manifestations of PA are low Hb,
hematocrit (HCT), and RBC levels.
• The diagnosis is based on the presence of
anemia, GI manifestations (weight loss,
appetite loss, nausea, vomiting, abdominal
distention, diarrhea, constipation, steatorrhea),
and neurologic disorders (paresthesias of feet
and hands, poor gate, memory loss, cognitive
problems, depression).
• Laboratory studies include a complete blood
count (CBC), peripheral smear, reticulocyte
count, Hb and HCT levels, serum iron level,
total iron-binding capacity, and serum ferritin
levels.
• In addition the Schilling test is the definitive
test for PA and is used to diagnose and
determine the cobalamin deficiency.
• The Schilling test measures the absorption of
orally administered radioactive vitamin B ₁2
(tagged with cobalt 60) before and after
parenteral administration of IF.
 Medical Management
Cobalamin/Vitamin B₁2 Therapy
• Clients with PA need both immediate treatment and
lifelong therapy with maintenance vitamin B₁2.
• The standard treatment is parenteral administration
of cobalamin (cyanocobalamin or
hydroxocobalamin) at 1000 mcg daily for 2 weeks
and then weekly until the HCT returns to normal.
Once the HCT is normal, monthly injections for life
are required.
• An intranasal form of cyanocobalamin
(Nascobal) is available as a nasal gel that is
self-applied weekly.
• The response to the injections is usually quick
and dramatic, often occurring within 24 to 48
hours. Within 72 hours, reticulocytes begin to
increase; by the end of the first week, the total
RBC count rises significantly.
• Iron Supplements
• Additionally the client may need oral or IV iron
supplements if the Hb level fails to rise in proportion
to an increased RBC count. Iron deficiency may be
an etiologic factor in pernicious anemia and must be
corrected if it is present.
• Iron deficiency anemia can also develop during
treatment of pernicious anemia.
• Injections of vitamin B₁2 may cause a rapid
regeneration of RBCs that depletes iron. As a result
the Hb level remains low, although the total RBC
count rises.
 Digestants
• Digestants may be given to enhance the
metabolism of vitamins; for example, HCl acid
may be diluted in water and given with meals
during the first few weeks of vitamin B ₁2
therapy.
• The diagnosis is confirmed by blood smear
and bone marrow examinations.
• HCl is probably present in the gastric juice.
• Neurologie manifestations are absent; and the
client responds favorably to a therapeutic trial
of 50 to 100 mg of folic acid administered
intramuscularly (IM) daily for 10 days.
 BLOOD LOSS
ACUTE BLOOD LOSS
In the case of trauma it may be impossible to
prevent the loss of blood. For the
postoperative patient, carefully monitor the
blood loss from various drainage tubes and
dressings and implement appropriate actions.
• CHRONIC BLOOD LOSS
• The sources of chronic blood loss are similar
to those of iron deficiency anemia (e.g.,
bleeding ulcer, hemorrhoids, menstrual and
postmenopausal blood loss).
• ANEMIA CAUSED BY INCREASED
ERYTHROCYTE DESTRUCTION
• The third major cause of anemia is termed
hemolytic anemia, a condition caused by the
destruction or hemolysis of RBCs at a rate that
exceeds production.
• Hemolysis can occur because of problems
intrinsic or extrinsic to the RBCs. Intrinsic
hemolytic anemias, which are usually hereditary,
result from defects in the RBCs themselves.
• Sickle cell disease
• Sickle cell disease (SCD) is a group of
inherited, autosomal recessive disorders
characterized by an abnormal form of
hemoglobin in the RBC. Because this is a
genetic disorder, SCD is usually identified
during infancy or early childhood. It is an
incurable disease that is often fatal by middle
age because of renal failure, infection,
pulmonary failure, and/or stroke.
 Sickling Episodes.
• The major pathophysiologic event of SCD is the sickling of RBCs.
• Sickling episodes are most commonly triggered by low oxygen
tension in the blood.
• Hypoxia or deoxygenation of the RBCs can be caused by viral or
bacterial infection, high altitude, emotional or physical stress,
surgery, and blood loss.
• Infection is the most common precipitating factor. Other events
that can trigger or sustain a sickling episode include dehydration,
increased hydrogen ion concentration (acidosis), increased plasma
osmolality, decreased plasma volume, and low body temperature. A
sickling episode can also occur without an obvious cause.
• Clinical Manifestations
• The effects of SCD vary greatly from person to person, the
severity of which may be due to genetic polymorphisms.
• Many people with sickle cell anemia are in reasonably
good health the majority of the time.
• The typical patient is anemic but asymptomatic except
during sickling episodes. Because most individuals with
sickle cell anemia have dark skin, pallor is more readily
detected by examining the mucous membranes.
• The skin may have a grayish cast. Because of the
hemolysis, jaundice is common and patients are prone to
gallstones (cholelithiasis
 Complications
• Infection is a major cause of morbidity and
mortality in patients with SCD.
• Pneumonia is the most common infection and
often is of pneumococcal origin.
• Acute chest syndrome is a term used to
describe acute pulmonary complications that
include pneumonia, tissue infarction, and fat
embolism. It is characterized by fever, chest
pain, cough, pulmonary infiltrates, and
dyspnea.
• Pulmonary infarctions may cause pulmonary hypertension, MI, HF, and
ultimately corpulmonale. The heart may become ischemic and enlarged,
leading to HF.
• Retinal vessel obstruction may result in hemorrhage, scarring, retinal
detachment, and blindness.
• The kidneys may be injured from the increased blood viscosity and the lack
of oxygen, and renal failure may occur. Pulmonary embolism or stroke can
result from thrombosis and infarction of cerebral blood vessels.
• Bone changes may include osteoporosis and osteosclerosis after infarction.
• Chronic leg ulcers can result from the hypoxia and are especially prevalent
around the ankles.
• Priapism (persistent penile erection) may occur if penile veins become
occluded
 Diagnostic Studies
• A peripheral blood smear may reveal sickled cells and
abnormal reticulocytes.
• Hemoglobin electrophoresis may be done to deter mine the
amount of hemoglobin S.
• Skeletal x-rays demonstrate bone and joint deformities and
flattening.
• Magnetic resonance imaging (MRI) may be used to diagnose
a stroke caused by blocked cerebral vessels from sickled cells.
• Doppler studies may be used to assess for deep vein
thromboses.
• Other tests may be indicated, such as a chest x-ray, to
diagnose infection or organ malfunction.
 Nursing Diagnoses
• Acute pain related to tissue hypoxia due to
agglutination of sickled cells within blood
vessels
• Risk for infection
• Risk for powerlessness related to illness-
induced helplessness.
• Deficient knowledge regarding sickle crisis
prevention
 Hemolytic anemia
Hemolytic anemia is an end result of
conditions that lead to hemolysis. Hemolysis,
the premature destruction of erythrocytes, can
result from physical damage, intrinsic
membrane defects, abnormal Hb, erythrocytic
enzymatic defects, immune destruction of
RBCs by macrophages, or hypersplenism.
• Acquired hemolytic anemia
Acquired hemolytic anemia results from
hemolysis of RBCs from extrinsic factors.
These factors can be separated into four
categories: (1) macroangiopathic (physical
trauma), (2) micro angiopathic, (3) antibody
reactions, and (4) infectious agents and toxins.
• Macroangiopathic or physical destruction of
RBCs results from the exertion of extreme
force on the cells. Traumatic events causing
disruption of the RBC membrane include
hemodialysis, extracorporeal circulation used
in cardiopulmonary bypass, and prosthetic
heart valves..
• Microangiopathic destruction of RBCs is a
result of fragmentation of the cells as they try
to pass by abnormal arterial or venous
microcirculation. The RBCs are sheared as
they try to pass by excessive platelet
aggregation and/or fibrin polymer formation,
such as is seen in thrombotic
thrombocytopenic purpura (TTP) and
disseminated intravascular coagulation (DIC).
• Antibodies may destroy RBCs by the
mechanisms involved in antigen-antibody
reactions. The reactions may be of an
isoimmune or autoimmune type. Isoimmune
reactions occur when antibodies develop
against antigens from another person of the
same species. In blood transfusion reactions the
recipient's antibodies hemolyze donor cells.
Autoimmune reactions result when individuals
develop antibodies against their own RBCs.
• Infectious agents and toxins cause the fourth
type of acquired hemolytic disorder. Infectious
agents cause hemolysis in three ways: (1) by
invading the RBC and destroying its contents
(e.g., parasites such as in malaria), (2) by
releasing hemolytic sub stances (e.g.,
Clostridium perfringens), and (3) by
generating an antigen-antibody reaction (e.g.,
Mycoplasma pneumoniae). Various agents
may be toxic to RBCs and cause hemolysis.
 Treatment and management
• Acquired hemolytic anemias involve general
supportive care until the causative agent can be
eliminated or at least made less injurious to the
RBCs.
• For chronic hemolytic anemia, folate may need to
be replaced.
• To suppress the RBC destruction,
immunosuppressive agents may be used, such as
rituximab, a monoclonal antibody to B-cell CD20,
and eculizumab, a monoclonal antibody to
complement protein.
 Nursing Diagnoses
1. Fatigue related to decreased hemoglobin and
diminished oxygen-carrying capacity of the
blood.
2. Altered nutrition, less than body
requirements, related to inadequate intake of
essential nutrients.
3. Altered tissue perfusion related to inadequate
blood volume or hematocrit.
4. Noncompliance with prescribed therapy.