Iron deficiency anemia is a common global health problem affecting 30% of the population. It causes decreased work productivity and increases maternal, child, and infant mortality. Good dietary sources of iron include liver, oats, legumes, and cashew nuts. Iron deficiency can be treated with oral iron supplements taken for 8 weeks, while severe cases may require intravenous iron or blood transfusions. Prevention strategies include iron fortification of infant formula and treating iron deficiency in at-risk groups like adolescent females.

1. IRON DEFICIENCY ANEMIA
Dr.G.Bhanu Prakash

2. • Approximately 30 % of the global population
suffers from iron-deficiency anemia.
• Most cases are seen in developing countries.

3. • Iron deficiency anemia causes
1. Decreases in Work productivity.
2. Increase in Maternal mortality
3. Increase in Child mortality
4. Affects the child development.

4. SOURCES OF IRON:
• Clams – molluscan
• Liver, kidney, heart of animals.
• Shrimps.
• Oats , bran wheat
• Cashew nut, almonds, apricot .
• Cereals , pulses , legumes.

5. BODY REQUIREMENT:
• 0.8 – 1 mg of iron must be absorbed everyday
for normal functioning in children below 15
yrs of age.

6. ABSOPTION:
• It mainly occurs in the duodenum.
• Absorption of dietary iron is assumed to be
about 10% of the intake; so the daily diet
should contain at least 8-10 mg of iron.
TRANSPORT
• Transferrin protein helps in the transport of
iron in the circulation.

7. STORES:
• Ferritin is an intracellular iron-storage protein.
• Iron binds to ferritin and is stored in the cells.
Ferritin that is not combined with iron is called
apoferritin.
• The body of a newborn infant contains about
0.5 g of iron, whereas the adult content is
estimated to be 5 g.

8. • An infant is in a precarious (uncertain)
situation with respect to iron. Should the diet
become inadequate or external blood loss
occur, anemia ensues rapidly.
• Adolescents also are susceptible to iron
deficiency because of high requirements due to
the growth spurt, dietary deficiencies, and
menstrual blood loss.

9. ETIOLOGY
• In term infants iron deficiency anemia is
unusual before 6 mo and usually occurs at
9-24 mo of age.
• Low birth weight and unusual perinatal
hemorrhage are associated with decreases in
neonatal hemoglobin mass and stores of iron.

10. • Prolonged consumption of large amounts of
cow's milk ** (> 650 ml /day) along with
foods not supplemented with iron.
• Blood loss must be considered as a possible
cause in every case of iron-deficiency anemia,
particularly in older children.

11. • Occult bleeding may be caused by a lesion of
the gastrointestinal tract, such as milk protein-
induced inflammatory colitis, inflammatory bowel
disease, peptic ulcer, Meckel diverticulum, polyp, or
hemangioma.
• Hook worm infestations.
• H. pylori infection.
• Chronic diarrhea in early childhood.

12. • Intense exercise especially in high schools
girls results in iron depletion.
• Delayed clamping of the umbilical cord
(2 min) in developing countries may reduce
the incidence of iron deficiency.

13. • In the advanced stages of iron deficiency
anemia there are changes in the mucosa of the
GIT , like the blunting of the villi , this causes
bleeding and also prevents further iron
absorption thereby worsening the anemia.

14. CLINICAL MANIFESTATIONS
• PALLOR is the most important sign of iron
deficiency anemia.
• There are high rates of false positive and false
negative results for palmer, nail bed and
conjunctival pallor which vary according to
the degree of anemia.

15. • PAGOPHAGIA, the desire to ingest unusual
substances such as ice or dirt, may be present.
• PLUMBISM may occur on ingesting lead-
containing substances.
• When the hemoglobin level falls to <5 g/dl,
IRRITABILITY and ANOREXIA are
prominent.

16. • Tachypnea, Tachycardia, weakness, cardiac
dilation, dyspnea on exertion, systolic murmurs,
CCF all are seen in severe anemia.
• Child will have EVIDENT SIGNS OF POOR
NUTRITION.
• Iron deficiency anemia or iron deficiency with out
anemia affects the attention span, alertness and
learning in both infants and adolescents
( improvement was noted within 8 weeks of therapy).

17. INVESTIGATIONS
• Serum ferritin gives us an accurate estimate
of the serum iron stores and their levels are
decreased in iron deficiency.
• Serum iron levels decrease.
• Serum transferrin levels increase ( i.e the
iron binding capacity increases) and also the
serum transferrin receptors.
• The percentage saturation of transferrin
falls below normal.

18. • The MCV, MCH, MCHC are all decreased.
• As the deficiency progresses there is presence of
microcytosis, hypochromia, poikilocytosis and
increase RBC distribution width (RDW).
• Absolute reticulocyte counts indicate an
insufficient response to anemia.

19. The Bone marrow examination
• Hypercellular with erythroid hyperplasia.
• The normoblasts may have scanty, fragmented
cytoplasm with poor hemoglobination.
• Leukocytes and megakaryocytes are normal.
• There is no stainable iron in marrow reticulum
cells.
In about 1/3 of cases, occult blood can be
detected in the stool.

20. DIFFERENTIAL DIAGNOSIS
1. Alpha and Beta thalassemia trait and other
hemoglobinopathies ( in them the RBC count is
elevated above normal despite the presence of a mild
anemia and microcytosis, whereas in iron deficiency
anemia RBC count usually decreases long with the
reduced hemoglobin and MCV.
Another difference between alpha and B-thalassemia
trait and iron deficiency is that the RDW is elevated
in iron deficiency.

21. 2. The anemia of chronic disease (ACD) and
infection usually is normocytic, although
occasionally it may be slightly microcytic.
Here serum ferritin levels are normal or
elevated (ferritin is an acute phase reactant).
• The serum transferrin receptor (TfR) level
is elevated in iron deficiency and is within the
normal range in anemia of chronic disease.

22. 3. In cases of Lead Poisoning associated with
iron deficiency the RBC’s are morphologically
similar, but
• Coarse basophilic stippling of the RBC’s often
is prominent.
• Elevated blood levels of lead, FEP- free
erythrocyte protoporphyrins levels and urinary
coproporphyrin levels .

24. TREATMENT
• Oral administration of simple ferrous salts
(e.g: sulfate, gluconate, fumarate) provides
inexpensive and satisfactory therapy.
• Older children and adolescents some times
have GI complaints (constipation )
• These can be over come by giving water with
fibres , or giving iron with food though iron
absorption may decrease.

25. • Therapeutic dose should be calculated in terms
of elemental iron
• 4-6 mg/kg /day of elemental iron in 3
divided doses provides an optimal amount of
iron.

26. • Parenteral iron preparation (iron dextran)
can be given, but occasional complication
being anaphylaxis , another Parenteral form
ferric gluconate can be given IV having less
risk of anaphylaxis.
• Iron medication should be continued for 8 wk
even after the blood values return to normal.

27. • Family must be educated about the patient's
diet.
• Milk consumption should be limited to a
reasonable quantity, preferably 500 mL / 24hr
or less. This reduction has a dual effect: The
amount of iron-rich foods is increased, and
blood loss from intolerance to cow's milk
proteins are reduced.

28. • Blood transfusion is indicated only when the
anemia is very severe or when superimposed
infection may interfere with the response to
iron therapy.
• Severely anemic children with hemoglobin
values <4 g/dL should be given only 2-3 ml/kg
of packed cells at any one time (furosemide
also may be administered as a diuretic).

29. PREVENTION
1. Use of Iron fortified formula’s or cereals in
infants of high risk population, can reduce
the risk of iron deficiency anemia.
2. Adolescent females who develop iron
deficiency due to abnormal uterine blood
flow loss should be treated with iron and
hormone therapy.

30. THANK YOU