Microcytic normocytic and

macrocytic
By Dr Hodan Jama
02/12/2017
Hypochromic Microcytic Anemia
• Iron Deficiency Anemia
• Thalassemia Minor
• Lead Poisoning
Iron Deficiency Anemia

Etiology.
Dietary
▫ Infants fed cow’s milk when younger than
1 year of age,
▫ toddlers fed large volumes of cow’s milk
▫ menstruating teenage girls who are not
receiving supplemental iron
• chronic inflammatory diseases
Epidemiology

• the most common cause of anemia in the world,

• is about 9% in toddlers,
• 9% to 11% in adolescent girls,
• less than 1% in teenage boys.
• one third of children who are iron deficient
• Breastfed infants are less likely to have iron
deficiency than bottle-fed infants
Clinical Manifestations

• cardiovascular manifestations of anemia

• central nervous system (CNS) abnormalities
▫ (apathy, irritability, poor concentration)
• Poor muscle endurance
• gastrointestinal dysfunction
• impaired WBC and T-cell function
• Iron deficiency in infancy may be associated with
later cognitive deficits and poor school
performance.
Treatment

• healthy child, a therapeutic trial of iron is the best

• The response to oral iron includes
▫ rapid subjective improvement,
▫ especially in neurologic function within 24 to 48
hours
▫ reticulocytosis 48 to 72 hours
▫ increase in hemoglobin levels (4 to 30 days)
▫ repletion of iron stores (in 1 to 3 months).
•
• The usual therapeutic dose of 4 to 6 mg/day of
elemental iron induces an
▫ increase in hemoglobin of 0.25 to 0.4 g/dL/day (a
1%/day increase in hematocrit)
• If the hemoglobin level fails to increase within 2
weeks after institution of iron treatment, careful
re-evaluation
▫ for ongoing blood loss,
▫ development of infection,
▫ poor compliance,
▫ other causes of microcytic anemia is required
Prevention

• Bottle-fed infants should receive an iron-containing

formula until 12 months of age
• breastfed infants older than 6 months of age should
receive an iron supplement.
• introduction of iron-enriched solid foods at 6 months of
age, followed by a transition to a limited amount of cow’s
• milk and increased solid foods at 1 year
• Teenage girls who are menstruating should have a diet
enriched with iron-containing foods
• A vitamin with iron may also be used.
Thalassemia Minor
• Etiology and Epidemiology.
• α-Thalassemia and β-thalassemia minor are
common causes of microcytosis
• They are prevalent in certain ethnic groups
(Mediterranean, Southeast Asian, African
Americans)
• Individuals of Asian descent are at risk of having
three or four α genes deleted,
• resulting in hemoglobin H disease (γ4) or hydrops
fetalis with only Bart (α4) hemoglobin
Laboratory Testing.
• The thalassemia minor syndromes are
characterized by a mild hypochromic, microcytic
anemiawith a low absolute reticulocyte count
• The RBC count is usually elevated.
• As a result, if the mean corpuscular volume (MCV)
divided by the RBC count is less than 12.5
• the diagnosis is suggestive of thalassemia trait.
• The blood smear reveals only microcytosis with α-
thalassemia trait.
• Blood smears of β-thalassemia minor show
▫ microcytic RBCs.
▫ Target cells and basophilic stippled RBCs,
• The diagnosis is based on an elevation of
hemoglobin A2 and F levels in β-thalassemia.
• Molecular testing is indicated for identification
of more severe or unusual variants.
Treatment.
• No treatment is required for children with
thalassemia minor.
• However, children with hemoglobin H disease
(γ4), especially the
▫ Constant Spring variant or
▫ hydrops fetalis with only Bart (α4) hemoglobin,
• are likely to require chronic transfusion therapy.
Lead Poisoning

• Lead poisoning may be associated with a

hypochromic, microcytic anemia.
• Most patients have concomitant iron deficiency.
• The history of living in an older home
▫ (built before 1980) with chipped paint or lead dust
▫ should raise suspicion of lead poisoning,
▫ especially in a child with pica.
• Basophilic stippling on the blood smear is
common.
• Lead intoxication rarely causes hemolytic
anemia
• Detection by routine screening
• removal from exposure
• chelation therapy, and correction of iron
deficiency
▫ are crucial to the potential development of
affected children.
Normocytic Anemia

Etiology and Treatment

• Anemia is a common component of chronic
inflammatory disease.
• Hepcidin a protein made in the liver, plays a key
role in iron homeostasis
• Inflammation causes an increase in the production
of hepcidin
• interrupting the process of iron release by
macrophages and the absorption of iron from the
intestines leading to anemia
Anemia of inflammation

• May be normocytic or, less often, microcytic.

• This may pose a clinical challenge, when
children with inflammatory disorders associated
with blood loss
• In these circumstances, only a bone marrow
aspiration with staining of the sample for iron
can differentiate the two entities clearly
• Low ferritin levels indicate concurrent iron
deficiency.
• A trial of iron therapy is not indicated without a
specific diagnosis in children who appear to be
systemically ill.
• Bone marrow infiltration by malignant cells
commonly leads to a normochromic,
normocytic anemia.
• The mechanism by which neoplastic cells interfere with
RBC and other marrow cell synthesis is multifactorial.
▫ The reticulocyte count is often low.
▫ Immature myeloid elements may be released into the
peripheral blood because of the presence of the offending
tumor cells.
▫ An examination of the peripheral blood may reveal
lymphoblasts; when solid tumors metastasize to the marrow,
these cells are seldom seen in the peripheral blood.
▫ Teardrop cells may be seen in the peripheral blood.
▫ A bon marrow examination is frequently necessary in the
face of normochromic, normocytic anemia.
Congenital pure RBC aplasia (Diamond-Blackfan
syndrome)
• a lifelong disorder
• usually presents in the first few months of life or at birth
▫ with severe anemia and
▫ mild macrocytosis or a normocytic anemia.
• It is due to a deficiency of bone marrow red blood cell
precursors
• More than a third of patients have short stature.
• Many patients (50% to 66%) respond to corticosteroid
treatment,
• but must receive therapy indefinitely.
• Patients who do not respond to corticosteroid
treatment are transfusion dependent
• They are at risk of the multiple complications of
long-term transfusion therapy,
▫ especially iron overload.
• These patients have a higher rate of developing
leukemia or other hematologic malignancies
Transient erythroblastopenia of childhood
• A normocytic anemia caused by
• suppression of RBC synthesis,
• usually appears after 6 months of age in an
otherwise normal infant.
• Viral infections are thought to be the trigger,
although the mechanism leading to RBC aplasia is
poorly understood.
• The onset is gradual, but anemia may become
severe.
• Recovery usually is spontaneous.
• Differentiation from Diamond-Blackfan
syndrome,
• in which erythroid precursors also are absent or
diminished in the bone marrow, may be
challenging.
• Transfusion of packed RBCs may be necessary if
the anemia becomes symptomatic before
recovery.
Aplastic crises
• may complicate any chronic hemolytic anemia.
• These periods of severe reticulocytopenia,
leading to
▫ an acute exacerbation of the anemia,
▫ may precipitate cardiovascular decompensation.
• Human parvovirus B19 infects erythroid
precursors and shuts down erythropoiesis.
• Transient erythroid aplasia is without
consequence in individuals with normal RBC
survival.
• Recovery from parvovirus infection in hemolytic
disease is spontaneous
▫ but patients may need transfusion if the anemia is
severe.
Macrocytic Anemia
• Magaloblastic anemia
▫ Vitamin 12 deficiency
▫ Folate deficiency
• Non magaloblastic anemia
▫ Chemotharpy drugs
▫ Liver disease
▫ Retuculocytosis
▫ hypothyroidism
Macrocytic Anemia
• Macrocytosis is a descriptive term for red blood
cell (RBC) size larger than the normal range.
• It may be caused by abnormalities of RBC
production in the bone marrow,
• altered RBC membrane composition, or an
increase in the percentage of reticulocytes, which
are larger than mature RBCs
Vitamin B12 deficiency
causes
• Vitamin B12 deficiency
▫ Pernicious anemia
▫ Ileac resection
▫ Strict vegetarian
▫ Abnormal intestinal transport
▫ Congenital intrinsic factor or
▫ transcobalamin deficiency
Folate deficiency
causes
• Folate deficiency
▫ Malnutrition
▫ Malabsorption
▫ Antimetabolite
▫ Chronic hemolysis
▫ Phenytoin
▫ Trimethoprim/sulfa
Others couses
• Hypothyroidism
• Chronic liver disease
• Down syndrome
Vitamin B12
• Vitamin B12 is Found
▫ Liver, Kidney ,Fish,Egg and milk
• Stores in the liver
• The body needs about 1ug daily
• Marrow failure
▫ Myelodysplasia
▫ Fanconi anemia
▫ Aplastic anemia

• Drugs
▫ Alcohol
(zidovudine)
Etiology
• Inadequate dietary intake
• Malabsorption
• Absence of VB12 trasport
• Giardia lambia
Clinical diagnosis
• Weakness
• fatigue
• failure to thrive
• Restlessness
• Pallor
• Glossities
• Jaundice
• Diarrhea
• Vomiting
• Neurologic symptoms
• Paresthesias
• Hypotonia
• Seizure
• Devolopmental delay
Diagnosis

• Neutrophils large and hyper segmented

• High level of methylmalonic acid and
homocysteine
• Low leval of VB12
• LDH also is high
Treatment

• Intravenous administration of VB12

• Monthly IM 1mg of VB12
• If neurological symptoms are present
▫ Give 1mg IM daily for at least 2wks
Folic acid deficiency
• Folate are getting many food
▫ Green vegetable
▫ fruits
▫ liver and
▫ kidneys
Etiology

• Inadequate folate
• Decreased folate absorption
• Congenital desease
Clinical of the disease

Same as VB12 deficiency

Laboratory

• Low reticulocyte count and nucleated RBC

• High neutrophils with hyper segmented
• Normal iron level and B12
• High HDL level
Treatment
• Folic acid PO or parentally
• At 0.5-1mg/day
• Should be continue 3-4 wks