HEMATOLOGICAL ALTERATIONS

Aplastic Anemia
DEFINITION

• Is a condition wherein injury to or

abnormal expression of the stem cells
in the bone marrow results in the
production of inadequate numbers of
erythrocytes, leukocytes, and platelets.
• Aplastic anemia
ETIOLOGY

• Can be categorized as either hereditary

or acquired
• Fanconi’s anemia (FA) – the
hereditary form of aplastic anemia, is a
rare autosomal recessive disorder that
develops early in life and is
accompanied by multiple congenital
abnormalities.
• Acquired aplastic anemia – can be
either idiopathic or due to secondary
causes.
• Idiopathic aplastic anemia - is rare in
children and adolescents, and for this
reason, secondary causes should
always be investigated in these age
groups.
• Autoimmune suppression of blood
cell production – is the most common
cause of aplastic anemia.
• Common toxic and pharmacologic
causes of aplastic anemia:

Toxic agents

• Benzene
• Toluene
• Insecticides
• Arsenic
Pharmacologic Agents

• Antibiotics
– Chloramphenicol
– Sulfonamides

• Anti-inflammatory agents
– Gold salts
– Phenylbutazone
• Anticonvulsants
– Phenytoin (Dilantin)
– Mephenytoin (Mesantoin)
– Trimethadione (Tridione)
– Carbamazepine (Tegretol)

• Antimalarials
– Quinacrine
• Analgesics
– Pyridium

• Oral hypoglycemics
– Tolbutamide (Orinase)
PATHOPHYSIOLOGY

• Plastic anemia, which is pancytopenia with a fatty

or "empty" bone marrow, is remarkable for the
simplicity of its pathologic picture and the direct
derivation of its clinical manifestations.
• Although it is not a common disease, the drama of
an individual case and the larger consequences of its
associations give it considerable interest.
• That aplastic anemia is perhaps the most dreaded
idiosyncratic complication of drug treatment has
serious and often expensive consequences for drug
development, for risk assessment, for approval by
regulatory agencies, and in legal actions.
CLINICAL MANIFESTATIONS

• Increased bruising caused by the

decreased number of platelets.
• Child becomes more vulnerable to
infection because of the decreased
number of WBC’s.
• Once the RBC’s have decreased in
number, the signs and symptoms of
anemia begin to manifest:
• Pallor
• Weakness
• Difficulty of breathing
• Impaired growth and development
• Acute myelogenous leukemia
DIAGNOSIS

• History and clinical manifestations are helpful but

laboratory tests are essential.
• A CBC with differential will show pancytopenia
(other initial lab. tests <page 823>)
• Bone marrow biopsy which will typically show
hypocellular marrow
• Bone marrow chromosome is used to differentiate
Fanconi’s anemia from acquired aplastic anemia
• Criteria for severe aplastic anemia

-Neutrophils <500µl
-Platelets <20,000µl
-Reticulocytes <1%
-Bone Marrow Cellularity <20%
TREATMENT

• Alleviate the underlying disorder or

prevent further exposure to the causal
agent
• If platelet count is less than 10,000
cells/µl, platelet transfusions are used
to increase the number of platelets in
circulation.
• Packed RBC’s should be administered
to increase the Hb level
• An intensive work-up should be initiated
in conjunction with administering broad-
spectrum antibiotics
• Bone marrow transplant or
immunosuppressive therapy
• Antithymocyte globulin (ATG) but slightly
less effective
• Androgen therapy
NURSING MANAGEMENT

• Assessment of the child for potential

health care needs
• A baseline temperature should be
recorded and the child monitored for
any fever or signs and symptoms of
infection.
• The nurse is also responsible for
implementing and teaching precautions
for preventing infection including proper
• Handwashing, aseptic technique, and
adequate fluid intake.
• Hospital care of a child with aplastic
anemia may include the administration
of platelets or other blood products, or
bone marrow transplantation.
• Emotional needs of the child and the
family should always be assessed.
• The child or other family members may
need education about aplastic anemia,
reassurance, or just a listening ear.