Iron-deficiency anemia is the most common nutritional disorder worldwide. It occurs when iron levels in the body are low and there is not enough iron to produce normal red blood cells. Symptoms can include pallor, fatigue, and irritability. Diagnosis involves blood tests showing low iron levels, smaller and fewer red blood cells. Treatment is oral iron supplementation which leads to improved hemoglobin levels within weeks. Prevention focuses on breastfeeding, iron-fortified formula for infants, and limiting milk intake after age 1.

2. Defenition
• Anemia is defined as a reduction of the
hemoglobin concentration or red blood cell
(RBC) volume below the range of values
occurring in healthy persons.
• “Normal” hemoglobin and hematocrit (packed
red cell volume) vary substantially with age
and sex .

3. NORMAL MEAN AND LOWER LIMITS OF NORMAL FOR HEMOGLOBIN,
HEMATOCRIT, AND MEAN CORPUSCULAR VOLUME
AGE (YR)
HEMOGLOBIN (G/DL) HEMATOCRIT (%)
MEAN
CORPUSCULAR
VOLUME (?M3)
Mean Lower Limit Mean
Lower
Limit
Mean
Lower
Limit
0.5-1.9 12.5 11.0 37 33 77 70
2-4 12.5 11.0 38 34 79 73
5-7 13.0 11.5 39 35 81 75
8-11 13.5 12.0 40 36 83 76
12-14 female 13.5 12.0 41 36 85 78
12-14 male 14.0 12.5 43 37 84 77
15-17 female 14.0 12.0 41 36 87 79
15-17 male 15.0 13.0 46 38 86 78
18-49 female 14.0 12.0 42 37 90 80
18-49 male 16.0 14.0 47 40 90 80

4. History and Physical Examination:
• As with any medical condition, a detailed history and
thorough physical exam are essential when evaluating
an anemic child.
• Important historical facts should include age, sex, race
and ethnicity, diet, medications, chronic diseases,
infections, travel, and exposures.
• A family history of anemia and/or associated
difficulties such as splenomegaly, jaundice, or early-age
onset of gallstones is also of consequence.
• There often are few physical symptoms or signs that
result solely from a low hemoglobin, particularly when
the anemia develops slowly.

5. • Clinical findings generally do not become apparent
until the hemoglobin level falls to <7-8 g/dL.
• Clinical features can include pallor, sleepiness,
irritability, and decreased exercise tolerance. Pallor can
involve the tongue, nail beds, palms, or palmar
creases.
• A flow murmur is often present.
• Ultimately, weakness, tachypnea, shortness of breath
on exertion, tachycardia, cardiac dilatation, and high-
output heart failure will result from increasingly severe
anemia, regardless of its cause.
History and Physical Examination:

6. Laboratory Studies:
• Initial laboratory testing should include
hemoglobin, hematocrit, and red cell indices
as well as a white blood cell count and
differential, platelet count, reticulocyte count,
and examination of the peripheral blood
smear.
• The need for additional laboratory studies is
dictated by the history, the physical, and the
results of this initial testing.

7. Differential Diagnosis:
• Anemia is not a specific entity but rather can result
from any of number of underlying pathologic
processes.
• In order to narrow the diagnostic possibilities, anemias
may be classified on the basis of their morphology
and/or physiology.
• Anemias may be morphologically categorized on the
basis of RBC size (mean corpuscular volume [MCV]),
and microscopic appearance.
• They can be classified as microcytic, normocytic, or
macrocytic based on whether the MCV is low, normal,
or high, respectively.

8. • Anemias may also be further divided on the basis
of underlying physiology.
• The two major categories are decreased
production and increased destruction or loss.
• Decreased RBC production may be a
consequence of ineffective erythropoiesis or a
complete or relative failure of erythropoiesis.
• Increased destruction or loss may be secondary
to hemolysis, sequestration, or bleeding.
Differential Diagnosis:

9. • The peripheral blood reticulocyte percentage or
absolute number will help to make a distinction
between the two physiologic categories.
• The normal reticulocyte percentage of total RBCs
during most of childhood is about 1.0%, with an
absolute reticulocyte count of 25,000-
75,000/mm3.
• Low or normal numbers of reticulocytes is
associated with relative bone marrow failure or
ineffective erythropoiesis.
• Increased numbers of reticulocytes represent
RBC destruction (hemolysis), sequestration, or
loss (bleeding).
Differential Diagnosis:

12. Iron-Deficiency Anemia:
• Iron deficiency is the most widespread and
common nutritional disorder in the world.
• It is estimated that 30% of the global
population suffers from iron-deficiency
anemia, and most of them live in developing
countries.
• In the USA, 9% of children ages 12-36 mo are
iron deficient, and 30% of this group have
progressed to iron-deficiency anemia.

13. Etiology:
• Most iron in neonates is in circulating
hemoglobin.
• As the relatively high hemoglobin
concentration of the newborn infant falls
during the first 2-3 mo of life, considerable
iron is reclaimed and stored.
• These reclaimed stores usually are sufficient
for blood formation in the first 6-9 mo of life
in term infants.

14. • Dietary sources of iron are especially important in
these infants.
• In term infants, anemia caused solely by inadequate
dietary iron usually occurs at 9-24 mo of age and is
relatively uncommon thereafter.
• The usual dietary pattern observed in infants and
toddlers with nutritional iron-deficiency anemia in
developed countries is excessive consumption of
bovine milk (low iron content, blood loss from milk
protein colitis) in a child who is often overweight.
• Worldwide, undernutrition is usually responsible for
iron deficiency.
Etiology:

15. • Blood loss must be considered as a possible
cause in every case of iron-deficiency anemia,
particularly in older children.
• About 2% of adolescent girls have iron-
deficiency anemia, due in large part to their
adolescent growth spurt and menstrual blood
loss.
Etiology:

16. Clinical Manifestations:
• Most children with iron deficiency are asymptomatic
and are identified by recommended laboratory
screening at 12 months of age or sooner if at high risk.
• Pallor is the most important clinical sign of iron
deficiency but is not usually visible until the
hemoglobin falls to 7-8 g/dL.
• In mild to moderate iron deficiency (i.e., hemoglobin
levels of 6-10 g/dL), compensatory mechanisms may
be so effective that few symptoms of anemia aside
from mild irritability are noted.

17. • When the hemoglobin level falls to <5 g/dL,
irritability, anorexia, and lethargy develop, and
systolic flow murmurs are often heard.
• As the hemoglobin continues to fall,
tachycardia and high output cardiac failure
can occur.
Clinical Manifestations:

18. • Iron deficiency has nonhematologic systemic effects.
The most concerning effects in infants and adolescents
are impaired intellectual and motor functions that can
occur early in iron deficiency before anemia develops.
• There is evidence that these changes might not be
completely reversible after treatment with iron,
increasing the importance of prevention.
• Pica, the desire to ingest non-nutritive substances, and
pagophagia, the desire to ingest ice, are other systemic
symptoms of iron deficiency.
• The pica can result in the ingestion of lead-containing
substances and result in concomitant plumbism.
Clinical Manifestations:

19. Laboratory Findings:
• In progressive iron deficiency, a sequence of
biochemical and hematologic events occurs
• Clinically, iron deficiency anemia is not
difficult to diagnose.
• First, tissue iron stores are depleted. This
depletion is reflected by reduced serum
ferritin, an iron-storage protein, which
provides an estimate of body iron stores in the
absence of inflammatory disease.

20. • Next, serum iron levels decrease, the iron-
binding capacity of the serum (serum transferrin)
increases, and the transferrin saturation falls
below normal.
• As iron stores decrease, iron becomes unavailable
to complex with protoporphyrin to form heme.
Free erythrocyte protoporphyrins (FEPs)
accumulate, and hemoglobin synthesis is
impaired.
• At this point, iron deficiency progresses to iron-
deficiency anemia.
Laboratory Findings:

21. • With less available hemoglobin in each cell, the
red cells become smaller.
• This morphologic characteristic is best quantified
by the decrease in mean corpuscular volume
(MCV) and mean corpuscular hemoglobin (MCH).
• Increased variation in cell size occurs as
normocytic red cells are replaced by microcytic
ones; this variation is quantified by an elevated
RBC distribution width (RDW).
• The red cell count (RBC) also decreases.
Laboratory Findings:

22. • The reticulocyte percentage may be normal or moderately
elevated, but absolute reticulocyte counts indicate an
insufficient response to the degree of anemia.
• The blood smear reveals hypochromic, microcytic red cells
with substantial variation in cell size.
• Elliptocytic or cigar-shaped red cells are often seen .
• White blood cell count (WBC) is normal, and
thrombocytosis is often present.
• Thrombocytopenia is occasionally seen with very severe
iron deficiency, potentially confusing the diagnosis with
bone marrow failure disorders.
• Stool for occult blood should be checked to exclude blood
loss as the cause of iron deficiency.
Laboratory Findings:

23. Prevention:
• Iron deficiency is best prevented to avoid both its
systemic manifestations and the anemia.
• Breast-feeding should be encouraged, with the
addition of iron-fortified cereals after 4-6 mo of age.
• Infants who are not breast-fed should only receive
iron-fortified formula (12 mg of iron per liter) for the
first year, and thereafter bovine milk should be limited
to <20-24 oz daily.
• This approach encourages the ingestion of foods richer
in iron and prevents blood loss due to bovine milk–
induced enteropathy.

24. • When these preventive measures fail, routine
screening helps prevent the development of
severe anemia.
• Routine screening using hemoglobin or
hematocrit is done at 12 mo of age, or earlier
if at 4 mo of age the child is assessed to be at
high risk for iron deficiency.
Prevention:

25. Treatment:
• The regular response of iron-deficiency
anemia to adequate amounts of iron is a
critical diagnostic and therapeutic feature.
• Oral administration of simple ferrous salts
(most often ferrous sulfate) provides
inexpensive and effective therapy.

26. RESPONSES TO IRON THERAPY IN
IRON-DEFICIENCY ANEMIA
TIME AFTER IRON
ADMINISTRATION
RESPONSE
12-24 hr
Replacement of intracellular iron enzymes; subjective
improvement; decreased irritability; increased
appetite
36-48 hr Initial bone marrow response; erythroid hyperplasia
48-72 hr Reticulocytosis, peaking at 5-7 days
4-30 days Increase in hemoglobin level
1-3 mo Repletion of stores

27. • The therapeutic dose should be calculated in
terms of elemental iron.
• A daily total dose of 3-6 mg/kg of elemental
iron in 3 divided doses is adequate, with the
higher dose used in more severe cases.
• Ferrous sulfate is 20% elemental iron by
weight and is ideally given between meals
with juice, although this issue is usually not
critical with a therapeutic dose.
Treatment:

28. • Parenteral iron preparations are only used
when malabsorption is present or when
compliance is poor, because oral therapy is
otherwise as fast, as effective, and much less
expensive and less toxic.
• When necessary, parenteral iron sucrose and
ferric gluconate complex have a lower risk of
serious reactions than iron dextran.
Treatment:

29. • In addition to iron therapy, dietary counseling
is usually necessary. Excessive intake of milk,
particularly bovine milk, should be limited.
• If the anemia is mild, the only additional
study is to repeat the blood count
approximately 4 wk after initiating therapy.
• At this point the hemoglobin has usually risen
by at least 1-2 g/dL and has often normalized.
Treatment:

30. • If the anemia is more severe, earlier
confirmation of the diagnosis can be made by
the appearance of a reticulocytosis usually
within 48-96 hr of instituting treatment.
• The hemoglobin will then begin to increase
0.1-0.4 g/dL per day depending on the
severity of the anemia.
Treatment:

31. • Iron medication should be continued for 8 wk
after blood values normalize to re-establish
iron stores.
• Good follow-up is essential to ensure a
response to therapy. When the anemia
responds poorly or not at all to iron therapy,
there are multiple considerations, including
diagnoses other than iron deficiency.
Treatment:

32. • Because a rapid hematologic response can be
confidently predicted in typical iron deficiency,
blood transfusion is rarely necessary.
• It should only be used when congestive heart
failure is eminent or if the anemia is severe
with evidence of substantial ongoing blood
loss.
Treatment:

33. Thank
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