ANEMIA

ANEMIA
• A condition in which the hemoglobin concentration is
lower than normal.
• Usually not a condition but a sign that reflects an
underlying disorder- presence of fewer than normal RBCs
within the circulation.
• Causes:
- severe blood loss
- increased destruction( because of an overactive RES or
presence of abnormal RBCs from the bone marrow that
are destroyed by the RES eg sickle cell)
- decreased production of RBCs( due to deficiencies in co-
factors required for erythropoiesis, or due to bone
marrow suppression or bone marrow is not adequately
 Classification of anemia
• They are classified according to the underlying anomaly:
1. Deficiency in erythrocyte production( hypoploriferative
anemia)- the marrow cannot produce adequate numbers
of erythrocytes, as reflected by the low reticulocyte count.
2. Excessive destruction( hemolytic anemia)- stem from
premature destruction of RBCs resulting in liberation of
hemoglobin into the plasma. Hemolysis can result from an
abnormality with the RBC itself(sickle cell or G-6-PD
deficiency) or within the plasma( eg immune hemolytic
anemia), or from direct injury to the RBC within the
circulation ( eg hemolysis caused by mechanical heart
valve)
3. Excessive loss of RBCs from bleeding
 Clinical manifestations
• Specific manifestations vary depending on the severity of the anemia.
They include:
- Palpitations
- Dyspnoea
- Diaphoresis
- Weakness
- Anorexia
- Glossitis/ tongue is smooth and red( iron deficiency anemia) or beefy
red and sore( megaloblastic anemia)
- Fatigue and general malaise
- Pallor of the skin and mucous membranes
- Jaundice( esp. in metabolic and hemolytic)
- Angular cheilosis – in both types
- Cravings/ pica
 Diagnosis
• History taking( alcohol, family Hx, athletic endeavors,
nutrition) and physical examination
• Stool for occult blood
• Hemoglobin, hematocrit, reticulocyte count and RBC
indices( MCV)
• Iron studies( serum iron level, total iron binding capacity
and ferritin)
• Serum vitamin B12 and folate levels
• Erythropoietin levels
• CBC values-to determine whether anemia is an isolated
problem or part of another hematologic condition, such as
leukemia or myelodysplastic syndrome(MDS)
•
 Management
• Is directed toward correcting or controlling the cause of the
anemia; in respect to the type of anemia one is dealing
with.
• Nursing process:
- Activity intolerance related to weakness, fatigue and general
malaise
- Imbalance nutrition, less than body requirements, related to
inadequate intake of essential nutrients secondary to
glosssitis
- Ineffective tissue perfusion related to inadequate blood
volume or hematocrit
- Noncompliance with prescribed therapy related to side
 Complications
• Heart failure
• Paresthesia
• confusion
 1. Hypoploriferative anemias
a) Iron deficiency anemia
- Typically result from inadequate dietary intake of iron
for hemoglobin synthesis.
- Results when the iron stores have been depleted
- Inadequate iron stores can result from inadequate intake
as seen in vegetarians, or blood loss eg from intestinal
worms, bleeding from ulcers, gastritis, inflammatory
bowel disease or GIT tumors, or excessive menstrual
bleeding and pregnancy with inadequate iron
supplementation.
- Other causes can be from chronic alcoholism and
malabsorption syndrome seen after gastrectomy or with
 Clinical manifestations
• All other symptoms of anemia with addition to smooth, sore
tongue, brittle and ridged nails, and angular cheilosis( an
ulceration of the corner of the mouth).
DIAGNOSIS
- History taking and physical examination
- Bone marrow aspiration- most definitive method of diagnosis,
which detects low levels of or absent iron
- Hemoglobin levels – will be low due to its correlation with iron.
With reduced iron, there is reduced ferritin causing small RBCs
hence reduced MCV
- Hematocrit levels- low
- Stool for occult blood
- Serum iron levels- low, but high TIBC, which measures the
 Medical management
• Investigate the cause of iron deficiency( colonoscopy,
endoscopy, x-ray of GIT to detect ulcerations, gastritis,
polyps or CA.
• Iron supplements eg FeSo4, ferrous gluconate, ferrous
fumarate- for 6-12 months. They are in oral, IM and IV
preparations. A small test should be done before to avoid
anaphylactic reactions( small dose test)
• Health education on diet selection
• Encourage patient to continue with therapy. Take
supplementary 1 hour before meals or with meals –as
preferred, to reduce the severity of side
effects( constipation, cramping, nausea and vomiting)
• Avoid antacids and dairy products while taking iron
b) Aplastic anemia
- Caused by >a decrease in or damage to marrow stem cells
>damage to the microenvironment within the marrow
>replacement of the marrow with fat
- These result in markedly reduced hematopoiesis- affecting even
the rest of the cells
- Aplastic anemia can be congenital or acquired, or idiopathic
- Triggers/ predisposing factors of this anomaly are infections,
pregnancy, certain medications, chemicals, or radiation damage.
- Hypothesis- the body’s T- cells mediate an inappropriate attack
against the marrow, resulting in the bone marrow aplasia
• Manifestation – insidious and complications( infection,
purpura) may set in before Dx is made.
- Symptoms are those of anemia, plus signs of infection
eg throat infections, cervical lymphadenopathy or
splenomegaly. Others may be retinal hemorrhages
• Diagnosis – physical exam and history taking
- bone marrow aspirate which shows an
extremely hypoplastic marrow replaced with fat,
therefore few or no cells
• Medical management:
- Bone marrow transplant or peripheral stem cell
transplantation
- Immunosuppressive therapy – a combination of
antithymocyte globulin and cyclosporine. They prevent
the lymphocytes from destroying the stem cells
- Supportive therapy such as transfusion
- Assess client for signs of problems related to lack of
RBCs, WBCs, platelets eg bleeding, infection, and
intervene accordingly.
c) Megaloblastic anemia
- Defined as anemia due to deficiency of vitamin B12 or folic
acid or both, which are essential for normal DNA synthesis.
- RBCs produced are abnormally large and are called
megaloblastic RBCs
- Other cells derived from the myeloid stem cell are also
abnormal.
- A bone marrow analysis reveals hyperplasia( abnormal
increase in the number of cells), and the precursor cells
are also large
- Pancytopenia( a decrease in all myeloid- derived cells)
develops due to destruction of the myeloid cells within the
marrow
- On blood film: Hb may be as low as 4-5g/dl, the
WBC count 2,000 to 3,000/mm3, and the platelet
count less than 50,000/mm3. those cells released
into the circulation are often abnormal shaped.
The neutrophils are hypersegmented. The platelets
may be abnormally large. The RBCs are abnormally
shaped and the shapes may vary
widely( (poikilocytosis). Because the RBCs are very
large, the MCV is very high, usually exceeding
110um
• Folic acid deficiency occurs as follows:
- Folate stores are small and depleted quickly by
inadequate dietary intake( within 4 months)
- Alcohol increases folic acid requirements, and at the
same time, patients with alcoholism usually have a diet
that is deficient in vitamins
- Folic acid requirements are also increased in patients
with chronic hemolytic anemias and in women who are
pregnant, coz the need for erythrocyte production is
increased in these conditions
- Some patients with malabsorption disease of the small
bowel such as sprue may not absorb folic acid normally
• Vitamin B12 deficiency occurs as follows:
- Inadequate dietary intake-especially strict
vegetarians
- Faulty absorption from the GI eg in crohn’s disease
or after ileal resection or gastrectomy
- Absence of intrinsic factor( pernicious anemia),
produced by the parietal cells of the gastric mucosa
- Diseases involving the ileum or pancreas impairs
absorption which impairs absorption of the vitamin
- NB: the body has large stores for the vitamin , so it
takes a longer time before the symptoms show
• Clinical manifestations:
- Symptoms of lack of both are similar, and the two
anemias may coexist. They include:
- Neurological manifestations of vitamin B12
deficiency( weakness, paraesthesia, ataxia, muscle
weakness, confusion)
- Other signs of vit B deficiency- anorexia nausea,
vomiting and abdominal pain
- Pernicious anemia- smooth sore red tongue, mild
diarrhea, pallor
• Assessment and diagnosis
- Clinical manifestations
- Vitamin B12 deficiency- schilling test- small dose of oral
radioactive vitamin B 12, followed in a few hours by a large
nonradioactive parenteral dose of vitamin B12( this aids in
renal excretion of the radioactive dose). If the oral vitamin is
absorbed, more than 8% will be excreted in the urine( i.e the
radioactive vit B 12 stays within the GIT), the cause is GIT
malabsorption of the vitamin. Conversely, if the urine is
radioactive, the cause of the deficiency is not ileal disease or
pernicious anemia .
- CBC- shows macrocytic RBC and have abnormal shape
- Serum cobalamine levels and serum folate levels
- Gastroscopy and biopsy of gastric mucosa coz the potential
for gastric cancer is increased inpatients with pernicious
• Medical management
- Identification and management of the cause
- Folate deficiency- increasing the amount of folic acid in
the diet and administering 1gm of folic acid IM daily. For
alcoholics, supplementation should continue as long as
they are taking alcohol
- Vitamin B12 deficiency- vitamin B12 replacement. Oral
supplementation of the vitamin for vegetarians. Diet
may be comprising of fortified soy milk. Monthly
injection of vitamin B12 when the cause is due to lack of
intrinsic factor, usually 1000ug
- Small amounts of bland, soft food
- Offer assistance or assistive devices for walking
- Health education
d) Anemia in renal disease
- Caused by both a mild shortening of RBC
lifespan and a deficiency of erythropoietin
- Patients undergoing long-term hemodialysis
lose blood into the dialyzer and therefore may
become iron deficient. Also folic acid may be
lost in the dialysate
 2. Hemolytic anemias
• A premature destruction of erythrocytes occurring at a
faster rate than the bone marrow is able to compensate
for the loss.
• Can occur either intravascularly or extravascularly.
• Extravascularly, the spleen removes erythrocytes from the
circulation at an accelerated rate, usually due to some
perceived problem with the erythrocytes eg autoimmune
anemias and hereditary spherocytosis
• Intravascularly, erythrocytes lyse spilling their contents in
the plasma, as a result of an enzyme deficiency in the RBC
membrane or mechanical factors like prosthetic valves
• Causes are:
• Intrinsic problems- defects in the RBC themselves
caused by abnormal Hb eg sickle cell, G-6-PD
deficiency, or RBC membrane abnormalities. These
are inherited.
• Extrinsic- the RBCs are normal but damage is
caused by external factors such as trapping of cells
within the sinuses of the liver or spleen, antibody-
mediated destructions, toxins or mechanical injury
• Symptomatology:
- Jaundice
- Splenohepatomegally
- Other signs of anemia
• Management involves identification of the
cause and appropriate management
 3. Anemia due to bleeding
• Bleeding from gastrointestinal tract, epistaxis,
trauma, bleeding from genitourinary tract( eg
menorrhagia)