2. DEFINITION
Anemias are a group of diseases characterized by a
decrease in either the hemoglobin (Hgb) or the
volume of red blood cells (RBC’s) in blood to the
levels that are required for adequate tissue
oxygenation or which results in decreased oxygen-
carrying capacity of the blood.
Anemias are often a sign of underlying pathology.
Therefore a rapid diagnosis of the cause of the
anemia is essential.
3. Anemias can result from :
1) Inadequate RBC production.
2) Accelerated loss of RBC mass.
3) Manifestation of a host of systemic disorders such as
infection, chronic renal diseases or malignancy.
The term Anemia is not diagnosis but rather an
objective sign of diseases.
WHO defines Anemia in adult as hemoglobin levels
less than 13g/dl in males, less than 12g/dl in females
and less than 13g/dl in pediatrics.
5. ETIOLOGY
Etiology basically consist of three mechanism:
1) Reduced Hemoglobin synthesis which may be due
to lack of nutrients or bone marrow failure. This
leads to either reduced proliferation of precursors or
defective maturation of precursors or both.
2) Increased hemoglobin loss due to hemorrhage (red
cell loss) or heamolysis (red cell destruction)
3) Decreased red cell production i.e. disturbance in
stem cell proliferation or differentiation.
7. SIGNSAND SYMPTOMS
The Non-Specific signs and symptoms are:
1) Tiredness
2) Pallor (Unnatural lack of color in the skin)
3) Fainting
4) Exertional dyspnoea (Difficult respiration)
5) Tachycardia
6) Palpitation
7) Worsening Angina
8) Worsening cardiac failure
9) Exacerbation of Intermittent Claudication.(pain in leg
muscles because the blood supply is inadequate.)
8. Iron deficiencyAnemia (IDA)
Iron deficiency is the most common nutritional deficiency in
developing and developed countries and it is estimated that over 500
million people worldwide have IDA*
Hemoglobin consist of protein component with 2 alpha and 2 beta
chains.
Each chain linked to a heme group consisting of a porphyrin ring
structure with an iron atom chelated at its center which is capable of
binding oxygen.
Iron stores are 600-1200 mg for males and 100-400 mg for females,
only 0.5-1.0 mg/day is lost ; another 0.5-1.0 mg is lost daily during
menstruation.
Daily requirement of Iron 0.9mg in males, 2mg females, in pregnancy
it is 3-5mg and in infant it is 0.5mg.
*Data from the Third NHANES (National Health and Nutrition Examination Survey)
9. Etiology of IDA
Iron deficiency results from prolonged negative iron balance
or failure to meet increased physiologic iron need. The speed
of iron deficiency development depends on an individuals
initial iron stores and balance between iron absorption and
loss. Multiple etiologic factors are usually involved.
1) Blood loss (Menstruation, Gastrointestinal peptic ulcer,
Trauma)
2) Decreased absorption due to medication (e.g.. Drugs like
Tetracycline) or Gastrectomy or regional enteritis.
3) Increased requirement (Infancy, Pregnancy or lactating
females)
4) Impaired utilization (Heredity, decreased iron use)
10. Pathophysiology of IDA
Diminished total body iron content, developing in stages over a period of
negative iron balance
Iron depletion – Stage One
Iron deficient erthyropoiesis – Stage Two
Iron deficiency anemia – Stage Three
Stage One
Iron storage is exhausted - indicated by
decrease in serum ferritin levels No
anemia – RBC morphology is normal.
Stage Two
Insufficient iron to insert into
protoporphyrin ring to form heme –
Protoporphyrin accumulates in cell and
complexes with zinc to form ZPP No
anemia, no hypochromia, but slight
microcytosis may be decreased
Stage Three
All laboratory tests for iron status become
abnormal, Most significant finding is
microcytic, hypochromic anemia and there
is hyperplasia of erythroids.
11. Signs of IDA
1) Pale skin and mucous membrane
2) Painless glossitis (Inflammation of the tongue)
3) Angular stomatitis (Inflammation of the mucous membrane
of the mouth)
4) Koilonchia (Spoon shaped nails)
5) Dysphagia
6) Pica (Unusual cravings)
7) Atrophic Gastritis
8) Poikilocytes (misshapen red cells appear on the blood smear
as cigar-or pencil-shaped forms)
Chronic Iron
deficiency
13. Treatment of IDA
Aim of treatment is to correct the anemia and replenish iron
stores.
Treatment of IDA consist of dietary supplements and
administration of therapeutic iron preparation. It is best
absorbed from meat, fish and poultry. Beverages affect iron
absorption.
In most cases oral administration of iron therapy with soluble
iron salts is appropriate.
ORAL THERAPY
Iron sulphate, succinate, lactate, fumarate, glycine sulphate,
glutamate and gluconate are absorbed
The presence of mucopolyssacharides chelator substance
prevents the iron from precipitating and maintains the iron in
soluble form.
14. The dose of iron replacement therapy depends on the
patients ability to tolerate the administered iron.
The general recommendation is approximately administered
of 200mg of elemental iron daily normally in 2 to 3 divided
doses to minimize tolerability.
If patient cannot tolerate this than smaller amount of
elemental iron e.g. single 325mg tablet of iron sulphate is
sufficient.
Iron is preferably administered at least 1 hour before meal to
avoid food-drug interaction.
Many patient may take iron with food because they
experience nausea and diarrhea when administered on empty
stomach.
15.
16. Adverse Drug Reaction (ADR)
ADR to therapeutic dose of iron are Gastrointestinal in nature
1) Discoloration of feaces
2) Constipation and diarrhea
3) Nausea and vomiting
Drug Interaction
Drugs which decrease iron absorption
1) Aluminum, magnesium and calcium containing antacids
2) Tetracycline and doxycycline
3) Histamine (H2) antagonist
4) Proton pump inhibitor
5) Cholestyramine
17. Drugs affected by Iron
1) Levodopa ↓ (chelates with iron)
2) Methyldopa ↓ (decreases efficacy of methyldopa)
3) Levothyroxine ↓ (decreased efficacy of levothyroxine)
4) Penicillamine ↓ (chelates with iron)
5) Fluoroquinolones ↓ (forms ferric ion– quinolone complex)
6) Tetracycline and doxycycline ↓ (when administered within 2
hours of iron salt)
7) Mycophenolate ↓ (decreases absorption)
18. Causes of treatment failure for IDA
1) Poor patient adherence
2) Inability to absorb iron
3) Incorrect diagnosis
4) Continued bleeding
19. PARENTERAL IRON THERAPY
Parenteral therapy is taken when:
1) Evidence of iron malabsorption
2) Intolerance to orally administered iron
3) Long term non adherence
4) Patients who cannot take oral iron therapy
5) Patients with significant blood loss who refuse iron therapy.
PREPARATIONS
1) Iron Dextran; 50mg iron/ml
2) Sodium ferric gluconate; 2.5mg iron/5ml
3) Iron sucrose; 20mg iron/ml
20.
21. TRANSFUSIONS
Transfusion of allogenic blood is indicated in acute situations
of blood loss when hemodynamic support is needed.
Blood transfusion in chronic anemia can elevate Hb
concentration
An exception to this treatment option is patients who have
developed low Hct values over extended time periods. These
patients often demonstrate cardiac compromise after
transfusion despite Hct levels is in the 20% range. These
patients should receive iron therapy, followed by transfusion
only if necessary.
22. PATIENT CARE
Take iron products with or after meals – reduces the incidence
of nausea.
Patient should be told that their faeces may be of come dark
colored.
Discuss about the length of treatment and adherence to the
therapy.
23. MegaloblasticAnemia
Macrocytic anemia is divided into two types:
1. Megaloblastic anemia
2. Non megaloblastic anemia
The two major causes are:
1. Folate deficiency
2. Vitamin B12 deficiency
Pernicious anemia is a specific disease caused by
malabsoption of Vit. B12.
Important to distinguish B12 from folate deficiency.
24. Stages of B12 deficiency
Stage B12conc. Mean corpuscular Hb Signs &
vol. Symptoms
Normal Normal Normal Normal None
-ve bal. ” ” ” ”
Depletion of
Stores Slight ↓ ” ” Possible
B12 def. Moderate ↓ ↑ ” ”
Erythropoiesis
B12 def.
Anemia Severe ↓ ↑ ↓ Probable
25. Etiology of Vitamin B12 Deficiency
The three major causes are:
1. Inadequate intake
2. Malabsorption syndrome
3. Inadequate utilization
Deficiency occurs from inadequate intake or malabsorption.
The only dietary source of Vit. B12 (cyanocobalamin) is
from food of animal origin. It is present in meat, fish, eggs,
cheese and milk. Daily requirements are between 0.5-1.0 μg.
Malabsorption occurs if the distil ileum is removed during
stagnant loop syndrome, tropical sprue and fish tapeworm
infestation.
Drugs also cause malabsorption.
26. Pathophysiology of Vitamin B12
Vitamin B12 works closely with folate in the synthesis of
building blocks for DNA and RNA.
It is a water soluble vitamin obtained exogenously by
ingestion of meat, fish, poultry, diary products and
fortified cereals.
27. Most circulating
cobalamin complex
Free cobalamin
Binding complex
Cobalamin – R- Protein
complex
Release of cobalamin
Stomach
Dietary cobalamin
Complex secreated
into circulation
Mucosal cell receptors
(cubilin) in distal ileum
Cobalamin -Intrinsic factor
complex
Pepsin and HCL
R- Protein
Cobalamin -R- Protein complex
from Bile
Degradation by pancreatic
enzymes
Intrinsic factor
28. Gastrectomy – Vit. B12 deficiency
Vit. B12 deficiency Deposition of
methyltetrahydrofolate prevent DNA
synthesis
Defect in methylation reaction, needed for
myelin formation leads to neuropathy.
Alternate mechanism involves diffusion.
29. Investigation
Vit. B12
MMA, Hcy conc. and renal function
Schilling test and hematology
Clinical manifestations
• Macrocytosis
• Anisocytosis(cells of unequal size)
• Poikilocytosis(misshapen red cells)
• Thrombocytopenia
• Enlarged Spleen (spleenomegaly), Slight fever
• Mild jaundice and progressive neuropathy
31. Treatment
Goals
1. Reversal of hematologic manifestations
2. Replacement of body stores
3. Prevention or resolution of neurologic manifestations
Dietary intake
Oral administration of Vit.B12 (1-10µg/day cyanacobalamin)
Parenteral administration (100-1000ug deep sc)
Intranasal administration(400µg 3 times a week)
32. Adverse effect
1. Hyperuricemia and hypokalemia
2. Rebound thrombocytosis precipitate thrombotic events
3. Fluid retention in pateints with compromised CV status
4. Rare case of anaphylaxis with parenteral administration
33. FOLICACID Deficiency
Most common Vitamin deficiency
Critical in early pregnancy
The four major causes are:
1. Inadequate intake of folic acid
2. Decreased absorption
3. Hyper utilization
4. Inadequate utilization
5. Drugs (Azathioprine, methotrexate, phenytoin etc…)
Etiology of Folic acid Deficiency
34. Pathophysiology
GI cells and RBC
Methyltetrahydrofolate
monoglutamate
Folate
Monoglutamate
Polyglutamate
Dietary Folate
Dihydrofolate
Enzymes in the gut
Absorption
Methylation/ Reduction
Specific carrier
Methyl
Folate
Polyglutamate
DHF Reductase
35. Polyglutamate prevents folate leaking out of cell
Folate – coenzyme for DNA and RNA synthesis
Defective DNA synthesis affect GI cells and RBC – sore
tongue and anemia
Daily requirement- 50-100µg
In pregnancy additional 400µg/day recommended
Average amount of stores- 5-10mg
36. Clinical manifestation
1. Megaloblastosis
2. Glossitis
3. Diarrhea
4. Weight loss
5. Fatigue
6. Pallor
7. palpitation
8. Chronic folate deficiency predisposes patients to
thrombosis, depression and neoplasia
37. Investigation
1. Serum/erythrocyte Folate level
2. Increased plasma Hcy conc., RFT
3. Peripheral blood- large oval red cells
4. Anisocytosis and poikilocytosis
5. Hypersegmented neutrophils, thrombocytopenia
38. Therapy consist of :
1. Administration of exogenous folic acid
2. Replace body stores
3. Resolve signs and symptoms
Dietary intake
Oral preparations (1mg daily)
Parenteral administration(5mg/ml im/iv/sc)
Treatment
39. HemolyticAnemia
Hemolytic anemia decreases the life span of
erythrocytes
If the rate of destruction of the erythrocytes
exceeds the rate of production, then anemia
results
Wide range of hemolytic anemia with both
genetic and acquired disorders
40. Classification of HemolyticAnemia
1. Abnormalities of red blood cell interior
a.) Enzyme deficts
b.) Hemoglobinopathies
2. RBC membrane abnormilities
a.) Heridity spherocytosis
b.) Paroxyysmal nocturnal hemoglobinuria
c.) Spur cell anemia
3. Extrensic factors
a.) Splenomegaly
b.) Antibody immune hemolysis
c.) Microanglopathic hemolysis
d.) Infections, toxins etc.
Intra-
corpuscular
Extra-
corpuscular
Hereditary
Acquired
41. Etiology
1. Sickle cell anemia:
It is due to abnormal hemoglobin called hemoglobin S (HbS),
normal hemoglobin is usually HbA
α chains are normal and β chains are abnormal. HbS has
valine substituted for glutamic acid as the 6th amino acid in
the β polypeptide compared with HbA
The molecules of HbS polymerize into long chain and
precipitate inside the cells because of this RBC’s attain sickle
shape and become more fragile leading to hemolysis
Hemolysed sickle cell aggregate and block the blood vessels
leading to infarction.
42. 2. Thalassaemias
It is also known as Cooley’s anemia or Mediterranean anemia
(more common in Thailand and Mediterranean countries)
Due to inherited abnormalities of hemoglobin
It is of two types
1. α Thalassaemias
2. β Thalassaemias (more common)
Defective synthesis of globin genes
Production of α and β chains become imbalanced
Precipitation of polypeptide Precipitation of
polypeptide
chain in the immature RBC chain in the mature RBC
Disturbance in the process Hemolysis
43. α Thelassaemia (fetal life) β Thelassaemia
α chains are less, absent or β chains are less, absent or
abnormal with excess of abnormal with excess of
γ chains. α chains.
Defective Erythropoiesis and Hemolysis
G6PD deficiency:
G6PD is an erythrocyte enzyme that is indirectly involved in the
production of reduced Glutathione.
Glutathione is produced in response to and protects the red cells
from oxidizing reagents.
44. Pathophysiology
Normal 120 days life span of RBC (comes from its inherent
flexibilityin passing through the microvasculature and spleen
without disruption of cell membrane or sesquestration and
phagocytosis by reticuloendothelial cells)
Hemolysis RBC lifespan less than 120 days due to
1. Membrane defects
2. Alteration in hemoglobin solubility or stability
3. Changes in intracellular metabolic process
These changes can be intrinsic or extrinsic in origion
Intracorpuscular changes Extracorpuscular changes are
are genetically determined cause of hemolytic anemia
45. Hereditary spherocytosis: RBC’s lose their flexible biconcave
characteristics and become tight spheres destroyed by
reticuloendothilial cells, causing pigment bile stones, mild
jaundice and splenomegaly.
Sickle cell and Thelassaemia: Alteration in hemoglobin
solubility and stability cell deformation hemolysis
Some red cells in patients with sickle cell disease contain fetal
hemoglobin (HbF). These cells do not sickle.
G6PD Deficiency
G6PD deficiency i.e. decrease in G6PD
Decrease production of NADPH in erythrocytes
NADPH is needed to keep glutathione in reduced form
Hemoglobin in reduced from and helps erythrocytes deal with
47. Investigation
1. Sickle cell disease: abnormal hemoglobin electrophoresis
The proportion of hemoglobins is a useful monitoring parameter.
2. Thalassaemia: Hemoglobin electrophoresis
3. G6PD deficiency:
Treatment
1. Sickle cell anemia:
Patients with sickle cell disease have a high evidence of
Pneumococcal infections
Penicillin V (Phenoxymethyl penicillin): 250mg twice a day
usually for adults
Erythromycin being used for patients allergic to penicillin.
48. Administration of pneumococcal vaccine and haemophilus
influenza vaccine is now common
Increased proportion of HbF and decreased proportion of HbS on
the circulation
Drugs that may increase fetal Hb production
1. 5- Azacytidine
2. Cytarabine
3. Vinblastin
4. Hydroxycarbamide (Hydroxyurea) Cytotoxicity
5. Eruthropoietin
6. Short chain fatty acids (Valproate etc.)
Transfusions and exchange transfusions have also used to
decrease the proportion of Hbs. This is limited by the usual
complications of chronic infusions.
49. Iron overload the risk of blood borne virus transmission and
sensitization.
Strong opioids are required for pain relief. Morphine is a more
logical choice of opioids.
2. Thalassaemia:
No effective treatment for thalassemia
Desferrioxamine and Deferiprone are routinely needed.
Binds with free iron and Oral, but it is reported to cause
Iron bound to ferritin(serum reversible neutropenia so given
Ferritin reaches 1000ug/l) to pateints who are intolerant to
Desferrioxamine
50. Splenectomy
Drugs increases HbF: combination of drugs
Hydroxycarbamide (hydroxyurea) and erythropoietin
3. G6PD deficiency:
No specific treatment
During acute episodes the patient should be kept well
hydrated to ensure good urine output thus preventing Hb
damaging the kidney
Blood transfusion
51. Patient care
1. Sickle Cell
Encourage to take their prophylactic penicillin and folic acid
therapy regularly
Opioid addiction are prevented by giving analgesic
treatments recognize that the crises are extremely painful and
patient requires effective analgesia
2. Thalassaemia
Need to educate the patient regarding the cytotoxic nature of
hydroxycarbamide (hydroxyurea)
3. G6PD deficiency
Patients can be given a list of drugs to avoid
Drug therapy does not play a large part in the management.
52. Anemia of CHRONIC DISEASE
It is an hypoproliferative anemia that has traditionally been
associated with infections, inflammatory, hepatic disease or
neoplastic disease lasting for more than 1 to 2 months.
ACD is a response to stimulation of the cellular immune
system by various underlying disease processes. ACD
commonly develops in AIDS patients, especially those with
opportunistic infections or malnutrition, HIV infects
hematopoietic cells, which can lead to abnormal
hematopoiesis and bone marrow suppression. In addition, the
drugs used to treat AIDS and associated illness can cause bone
marrow suppression.
Etiology
53.
54. Pathophysiology
In this anemia RBC’s have shortened life span
Bone marrows capacity to respond to EPO is inadequate to
maintain normal Hb concentration
This anemia may be due to a block in release of iron from the
endothilial cells of the marrow
Cytokinins such as IL1, γ interferron and tumor necrosis
factor released during these illness may inhibit the production
or action of EPO or the production of RBCs
55. Signs and Symptoms
1. Fatigue
2. Breathlessness
3. Swollen feet
4. Chest pain
5. Decreased mental activity
Laboratory findings
1. Serum iron level
2. Bone marrow examination
56. Treatment
Recovery from the anemia usually occurs with resolution of
the underlying process. During inflammation Iron(Fe) therapy
is ineffective by either oral or parenteral route.
Exogenous EPO (recombinant human EPO or epoetin alpha)
has been used to stimulate erythropoiesis in patients with
chronic disease.
The epoetin alpha 150 units/kg given subcutaneously three
times weekly is effective.
Most patients tolerate epoetin alpha therapy well.
Iron deficiency can occur in patients treated with epoetin
alpha
57. However close monitoring of iron level is necessary during
epoetin alpha therapy
Oral iron supplementation should be given if transferrin
saturation drops to 20% or the serum ferritin level drops
below 100u/L
More common toxicities of epoetin alpha are fever, bone pain
and fatigue.
58. AplasticAnemia
It is group of disorders characterized by pancytopenia in
peripheral blood, vairiable hypocellularity in bone marrow,
absence of underlying malignent or myeloproliferative
disease.
ETIOLOGY
1. Congenital – rare
2. Acquired- virus or chemical
Other etiologies
Hepatitis, infectious mononucleosis, dengue and influenza
Regular exposure to irradiation
Major component of inherited conditions
59. Causes
Damage to the bone marrow's stem cells causes
aplastic anemia. When stem cells are damaged,
they don't grow into healthy blood cells.
The cause of the damage can be acquired or
inherited. Acquired aplastic anemia is more
common, and sometimes it's only temporary.
Aplastic anemia that's inherited is rare.
In more than half of the people who have aplastic
anemia, the cause of the disorder is unknown.
Some research suggests that stem cell damage
60. Acquired Causes
A number of diseases, conditions, and
factors can cause aplastic anemia,
including:
Toxins, such as pesticides, arsenic, and
benzene
Radiation and chemotherapy (treatments
for cancer)
Medicines, such as chloramphenicol (an
antibiotic rarely used in the United States)
Infectious diseases, such as hepatitis,
61. Autoimmune disorders, such as lupus and
rheumatoid arthritis
In some cases, cancer from another part of
the body can spread to the bone and cause
aplastic anemia.
62. Inherited
Causes
Certain inherited conditions can damage
the stem cells and lead to aplastic anemia.
Examples include Fanconi anemia,
Shwachman-Diamond syndrome,
dyskeratosis congenita, and Diamond-
Blackfan anemia
63. RISK FACTORS OF APLASTIC
ANEMIA
Aplastic anemia is a rare, but serious blood
disorder. In the United States, about 500–
1,000 people develop this type of anemia
each year.The disorder is two to three
times more common in Asian countries.
People of all ages can get aplastic anemia.
However, it's most common in adolescents,
young adults, and the elderly. Men and
women are equally likely to have it.
risk for aplastic anemia is higher if :
64. Taken certain medicines or had radiation or
chemotherapy treatment (treatments for
cancer)
Been exposed to toxins
Certain infectious diseases, autoimmune
disorders, or inherited conditions
65. SIGN AND SYMPTOMS
Low numbers of red blood cells, white
blood cells, and platelets cause most of the
signs and symptoms of aplastic anemia.
Signs and Symptoms of Low Blood Cell
Counts
The most common symptom of a low red
blood cell count is fatigue (feeling tired or
weak). Not having enough hemoglobin in
the blood causes fatigue. Hemoglobin is an
iron-rich protein in red blood cells that
66. A low red blood cell count also can cause
shortness of breath; dizziness, especially
when standing up; headache; coldness in
your hands or feet; pale skin, gums, and
nail beds; and chest pain.
If you don't have enough hemoglobin-
carrying red blood cells, your heart has to
work harder to circulate the reduced
amount of oxygen in your blood. This can
lead to arrhythmias, heart murmur, an
enlarged heart, or even heart failure.
67. White blood cells help fight infections.
Signs and symptoms of a low white blood
cell count include fevers, frequent
infections that can be severe, and flu-like
illnesses that linger.
Platelets stick together to seal small cuts
on blood vessel walls and stop bleeding.
People who have low platelet counts tend
to bruise and bleed easily, and the bleeding
may be hard to stop.
68. Types Common of bleeding linked to a low
platelet count include nosebleeds, bleeding
gums, pinpoint red bleeding spots on the
skin, and blood in the stool. Women also
may have heavy menstrual bleeding.
Paroxysmal Nocturnal Hemoglobinuria
About one-third of people who have
aplastic anemia have a condition called
paroxysmal nocturnal hemoglobinuria
(PNH). This is a red blood cell disorder. Most
69. OTHER SIGN SYMPTOMS
Aplastic anemia can cause signs and
symptoms that aren't directly related to
low blood cell counts. Examples include
nausea (feeling sick to your stomach) and
skin rashes.
Shortness of breath
Swelling or pain in the abdomen or swelling
in the legs caused by blood clots
Blood in the urine
Headache
70. Pathogenesis
It involves destruction inhibition or
impairment of stem cells, development of
abnormal micro cells or lack f hemopoietic co
factores.
Exogenous agents(virus,drug,metabolites)
inter the body
attaches to hemopoietic stem cells
agent-stem cell combination stimultus auto
immune procesm cells
71. Recovery may occurs with termination of
immune process and regeneration of patient
stem cells .
If auto immune process continues
immunosuppressive therapy alone may be
effective or followed by marrow
transplantation .
Drug included marrow aplasia –dose related
or idiosyncratic.
Chloramphenicol best drug given by oral,
72. Treatment
Treatments for aplastic anemia include blood transfusions,
blood and marrow stem cell transplants, and medicines.
These treatments can prevent or limit complications,
relieve symptoms, and improve quality of life.
In some cases, a cure may be possible. Blood and marrow
stem cell transplants may cure the disorder in people who are
eligible for a transplant. Removing a known cause of aplastic
anemia, such as exposure to a toxin, also may cure the
condition.
Needs of Treatment
People who have mild or moderate aplastic anemia may not
need treatment as long as the condition doesn’t get worse.
People who have severe aplastic anemia need medical
treatment right away to prevent complications.
People who have very severe aplastic anemia need emergency
medical care in a hospital. Very severe aplastic anemia can
be fatal if it's not treated right away.
73. Blood Transfusions
People who have aplastic anemia may need blood transfusions
to keep their blood cell counts at acceptable levels.
A blood transfusion is a common procedure in which blood is
given to you through an intravenous (IV) line in one of your
blood vessels. Transfusions require careful matching of
donated blood with the recipient’s blood.
Blood transfusions help relieve the symptoms of aplastic
anemia, but they’re not a permanent treatment.
Blood and Marrow Stem Cell Transplants
A blood and marrow stem cell transplant replaces damaged
stem cells with healthy ones from another person (a donor).
During the transplant, which is like a blood transfusion, you
get donated stem cells through a tube placed in a vein in your
chest. Once the stem cells are in your body, they travel to your
bone marrow and begin making new blood cells.
Blood and marrow stem cell transplants often cure aplastic
anemia in people who are eligible for this type of transplant.
74. Medicines
If you have aplastic anemia, your doctor may prescribe medicines to:
•Stimulate your bone marrow
•Suppress your immune system
•Prevent and treat infections
MedicinesTo Stimulate Bone Marrow
Man-made versions of substances that occur naturally in the body can
stimulate the bone marrow to make more blood cells. Examples of
these types of medicines include erythropoietin (e-RITH-ro-PO-e-tin)
and colony-stimulating factors.
These medicines have some risks.You and your doctor will work
together to decide whether the benefits of these medicines outweigh
the risks. If this treatment works well, it can help you avoid the need
for blood transfusions.
75. Medicines To Suppress the
Immune System
Three medicines—often given together—can
suppress the body’s immune system.They are
antithymocyte globulin (ATG), cyclosporine,
and methylprednisolone.
People who have aplastic anemia may need
long-term treatment with these medicines.
Medicines that suppress the immune system
can have side effects.They also may increase
the risk of developing leukemia (lu-KE-me-ah)
or myelodysplasia (MI-e-lo-dis-PLA-ze-a;
76. Ongoing Care
Treatment for aplastic anemia may cause side
effects or complications.
People who have aplastic anemia may be at
higher risk for infection due to low white
blood cell counts. For example, you may want
to:
Stay away from people who are sick and avoid
large crowds of people.
Avoid certain kinds of foods that can expose
you to bacteria, such as uncooked foods.
Wash your hands often.
Brush and floss your teeth and get regular
77. dose regimen
I.V ALG (10 mg/kg) for five alternate days.
I.V methyl prednisolone (8mg /kg/day) or
2mg/kg/day over 9 days.
Oral prednisolone (1.25mg/kg/day) from day
10 -15 declining to 0.1mg /kg /day from days
3-4.
