Simple approach to anemia and iron deficiency anemia

1. APPROACH TO ANEMIA AND IRON
DEFICIENCY ANEMIA
Dr Tushar Jagzape
Associate Professor,
Pediatrics,
AIIMS , Raipur

2. LEARNING OBJECTIVES:
 At the end of this lecture the students should be
able to:
 Define anemia
 Enlist classification of anemia
 Describe an approach to anemic child.
 Describe iron metabolism in short
 Enumerate causes of iron deficiency anemia
 Enlist clinical features
 Describe management of anemia

3. INTRODUCTION
Incidence – 71% in Urban children
84% in Rural children
Common in period of rapid growth.

4. DEFINITION OF ANEMIA
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• Hgb or hematocrit is two standard
deviation below the mean for that
particular age and sex.
* Tissue hypoxia occurs due to inadequate
oxygen carrying capacity of blood

5. Age Hemoglobin (gm/dl)
Mean -2SD
Birth 16.5 13.5
1-3 days 18.5 14.5
1 wk 17.7 13.5
2 wk 16.5 12.5
2 month 11.5 9
3-6 month 11.5 9.5
.5-2 yr 12 10.5
2-6yr 12.5 11.5
6-12yr 13.5 11.5
12-18yr(male) 14.5 13
12-18yr(female) 14 12
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6. WHO CUTOFF VALUES FOR THE DIAGNOSIS OF ANEMIA AT
DIFFERENT AGES
Age/ sex group Hb gm%
6 mo- 6 year < 11
6- 14 year < 12
Adult male < 13
Adult Female <12
Adult female (Pregnant) <11
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Grading
Mild – 8-12gm%
Moderate – 5-8gm%
Severe - < 5gm%

7. APPROACH
1. Is the patient anemic? If so
2. What is the cause of anemia? &
3. What is the type of anemia?
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8. IS THE PATIENT ANEMIC?
 Clinical symptoms and signs
 Pallor,
 Tiredness
 Lassitude
 Easy fatigability
 Weakness
 Shortness of breath
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9. WHAT IS THE CAUSE OF ANEMIA?
 Etiological classification of anemia
1. Anemia due to blood loss - Acute or chronic blood
loss
2. Anemia due to decreased production-
1. Nutritional deficiency
2. Hypoplastic or aplastic anemia
3. Bone marrow infiltration
4. Dyserytropoietic anemia
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10. 3. Anemia due to increased destruction-
1. Extracorpuscular – allo and isoimmune hemolytic anemia,
microangiopathic anemia, infections, hypersplenism
2. Intracorpuscular -
1. Red cell membranopathy-
2. Hemoglobinopathy
3. Enzymopathy
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11. CLASSIFICATION BASED ON RBC SIZE/
WINTROBE’S CLASSIFICATION
Normochromic Hypochromic
Normocytic
Acute H’ ge,
Hemolytic and
aplastic
Chronic H’ ge
Macrocytic Megaloblastic Liver diseases
Microcytic
Chronic
infections
Iron deficiency,
Thalessemia
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12. CLINICAL APPROACH TO AN ANEMIC
CHILD
1. Age
2. Sex/ Family history
3. Community
4. Dietary history
5. History of drug ingestion
6. Infections and infestations
7. Associated conditions –
hepatosplenomegaly, bleeding diasthesis, skeletal abnormality,
facies
8. Features due to anemia- pica, changes in epithelia cells etc
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13. CLINICAL APPROACH TO CHILD WITH ANEMIA
Anemia
No lymph nodes
No hepatosplenomegaly
With hepatosplenomegaly,
jaundice
With petechaie,lymphadenopathy,
&
hepatosplenomegaly
No petechiae or ecchymosis with petechiae or ecchymosis
Nutritional
Iron def. or megaloblastic
Pure red cell aplasia
Thalassemia trait
Red cell enzyme def.
Lead poisoning
Aplastic anemia
Bleeding disorder
Coagulation disorder
ITP,DIC
Thalessemia
Hemoglobinopathies
Liver disorders
Leukemia
Myeloprof. Dis
Infections
Infilterat.dis
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14. LABORATORY APPROACH
 Screening and confirmatory tests
1. peripheral smear examination in case of anemia
a) Size
b) Shape (poikilocyte) –
c) polychromasia – reticulocytosis
d) Heinz bodies – G6PD, thalassemia chemical injury etc.
e) Howell Jolly bodies – (nuclear remnants)
f) Parasite
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15. PS CTD
 Changes in WBC – leukoerthroblastic picture,
hypersegmented neutrophils
 Changes in Platelets –
2- Blood indices –
MCV
MCH
MCHC
RDW
3- Reticulocyte count – N -0.5-2%, & 2-6%
Corrected RC = Pt RC X Pt hematocrit
Normal hematocrit
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16. 3. WHAT IS THE TYPE OF ANEMIA?
 On basis of indices –
1. Microcytic hypochromic anemia-
Iron deficiency, abnormal hemoglobinopathies & thalassemia, lead
poisoning, sideroblastic anemia
2. Macrocytic anemia- Megaloblastic and non
megaloblastic
3. Normocytic normochromic anemia
post hemorrhagic, hemolytic anemia, renal and encocrinal
disorders
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17. SPECIAL INVESTIGATIONS OR
CONFIRMATORY TESTS
 Serum iron
 TIBC
 Serum ferritin
 Serum B12, folic acid
 Hb electrophoresis
 Enzyme assay
 Bone marrow examination
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18. IRON DEFICIENCY ANEMIA
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19. INTRODUCTION
 Most common hematologic disease of infancy
and childhood.
 Prevalence – 30% of the global population.
 Deleterious health conditions-
 Work productivity
 Severe anemia and child mortality
 Severe anemia and maternal mortality
 Iron deficiency anemia and child development.
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20. IRON METABOLISM
 1mg of iron/day – positive iron balance.
 Newborn infant -0.5g iron
 Adult – 5 gm iron
 0.8- 1mg/day absorption
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21. IRON METABOLISM CTD
 10% of dietary iron is absorbed.
 Dependent on –
 Extraluminal factors
 Intraluminal factors – net iron absorption increases with
↑ in dietary iron, but proportion ↓.
 Ferrous salts (Fe++), better absorbed than Fe+++
 Heme iron is better absorbed than non- heme.
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 Absorption inhibitors
 Phosphates
 Phytates
 Calcium salts
 Milk
 Egg
 Tannic acid
 Absorption facilitators
 Lactose
 Ascorbic acid
 Fruit jucies
 Amino acids (cystine,
lysine and histidine)
 HCl
Site – duodenum and upper jejunum

23. MECHANISM OF ABSORPTION:-
 Mucosal uptake
 Non heme iron – 2 transportors.
 Membrane associated cytochrome B –reduce Fe+++
to Fe++
 Divalent metal transporter 1 (DMT1) moves non
heme iron across the apical membrane.
 Absorbed iron + apoferritin = ferritin (storage
form of iron)
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24.  Transfer from mucosal cells to the plasma
 In the plasma iron combine with transferrin.
 It is a glycoprotein --- synthesised in the liver.
 1 molecule binds with 2 atoms of iron - TIBC
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26. CELLULAR UPTAKE OF IRON
 Transferrin receptor – glycoprotein present in
erythroid cells, placenta and liver cells.
 Circulating transferrin bind to the receptor and
release iron to the cell.
 Iron stores
– reticuloendothelial cells as ferritin
- bone marrow – hemosiderin granules
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27. ETIOLOGY
1. Low iron stores
2. Reduced iron intake
3. Excessive losses of iron from the body
4. Decreased iron absorption
5. Increased iron demand
6. Defective iron metabolism
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28. CLINICAL MANIFESTATIONS
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 Pallor
 Irritability , decrease
attention span
 Easy fatigability
 Failure to thrive
 Frequent infections
 Palpitation
 Cardiomegaly and
murmur
 Atrophied papillae,
 Thin, brittle , flat or
coiled nails.
 PICA

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31. DIFFERENTIAL DIAGNOSIS
 Other microcytic hypochromic anemias
 α and β thalassemia trait and other
hemogobinopathies
 Anemia of chronic diseases
 Lead posioning
 Sideroblastic anemia
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32. INVESTIGATION
Hb and CBC
Peripheral
smear-
anisocytosis,
microcytes, pencil
cells, hypochromia.
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33.  Indices- MCV < 80 fl, MCH < 27pg, MCHC < 33%
 RDW – N – 14.5%. Highly sensitive – 90-100%
Low specificity – 50-70
 Serum Ferritin – body iron stores - <12 ng/ml is highly
specific.
* no information about magnitude of ID
* level is increased in chronic disorders
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34.  Serum iron,TIBC & TS – Sr iron – diurnal variation –
peaks in morning and decrease in evening.
- TIBC – increased and
- Transferrin saturation is < 16%
 Free Erythrocyte Protoporphyrin (FEP)
 Soluble Transferrin Receptor (STfR) –
 STfR- ferritin complex. Most sensitive method to
differentiate IDA from ACD
 If it is > 4 it indicates IDA; if < 1 indicates chronic
disease.
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35.  Reticulocyte hemoglobin content
 Molecular gentics of iron deficiency
 Stainable iron in the bone marrow
 Response to therapy –
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37. TREATMENT-
 Deworming
 Change in dietary habits – meat, liver, kidney, egg yolk,
green vegetables and fruits.
 Wearing shoes are important measures.
 Iron therapy –
 Oral iron – Ferrous sulphate (20%), Fumarate
(33%),
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38.  Iron polymaltose complex, iron aminoacid
chelates (conjugates of Fe++ or Fe+++
with amino acids), carbonyl iron.
 Sprinkler – microencapsulated FeSO4 or
ferrous fumarate
 Parentral iron – iron dextran or ferric gluconate .
Iron (mg)= Wt in kg X Hb deficit (g/dl) X 4
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39. RESPONSE TO IRON THERAPY
Time Response
12-24 hrs ↓irritability, ↑appetite
36-48 hrs Initial BM response,Erythroid
hyperplasia
48-72 hrs Reticulocytosis, peak at 5-7 days,
4-30days ↑ in Hb level
1-3 months Repletion of stores
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40.  Failure of iron therapy –
 Blood transfusion
 Prevention –
1. Supplementation with medical iron- Term
babies after 4-6 months and preterm after
2 months.
2. Dietary modification and
3. Fortification of foods
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42. Compound % if elemental iron
Carbonyl iron 100
Ferric ammonium citrate 18
Ferrous bisglycinate 20
Ferrous fumarate 33
Ferrous gluconate 12
Ferrous sulphate 20
Ferrous sulphate dry 30
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