Approach to anemia and iron deficiency anemia
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Transcript of Approach to anemia and iron deficiency anemia
APPROACH TO ANEMIA AND IRON DEFICIENCY ANEMIADr Tushar JagzapeAssociate Professor,Pediatrics,AIIMS , Raipur
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
INTRODUCTIONIncidence – 71% in Urban children
84% in Rural children Common in period of rapid growth.
DEFINITION OF ANEMIA05/02/2023
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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
Age Hemoglobin (gm/dl)Mean -2SD
Birth 16.5 13.51-3 days 18.5 14.51 wk 17.7 13.52 wk 16.5 12.52 month 11.5 93-6 month 11.5 9.5.5-2 yr 12 10.52-6yr 12.5 11.56-12yr 13.5 11.512-18yr(male) 14.5 13
12-18yr(female) 14 12
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WHO CUTOFF VALUES FOR THE DIAGNOSIS OF ANEMIA AT DIFFERENT AGESAge/ sex group Hb gm%6 mo- 6 year < 116- 14 year < 12Adult male < 13Adult Female <12Adult female (Pregnant) <11
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GradingMild – 8-12gm%Moderate – 5-8gm%Severe - < 5gm%
APPROACH1. Is the patient anemic? If so2. What is the cause of anemia? &3. What is the type of anemia?
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IS THE PATIENT ANEMIC? Clinical symptoms and signs
Pallor, Tiredness Lassitude Easy fatigability Weakness Shortness of breath
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WHAT IS THE CAUSE OF ANEMIA? Etiological classification of anemia1. Anemia due to blood loss - Acute or chronic
blood loss2. Anemia due to decreased production-
1. Nutritional deficiency2. Hypoplastic or aplastic anemia3. Bone marrow infiltration4. Dyserytropoietic anemia
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3. Anemia due to increased destruction-1. Extracorpuscular – allo and isoimmune hemolytic
anemia, microangiopathic anemia, infections, hypersplenism
2. Intracorpuscular - 1. Red cell membranopathy- 2. Hemoglobinopathy3. Enzymopathy
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CLASSIFICATION BASED ON RBC SIZE/ WINTROBE’S CLASSIFICATION
Normochromic Hypochromic
NormocyticAcute H’ ge,
Hemolytic and aplastic
Chronic H’ ge
Macrocytic Megaloblastic Liver diseases
Microcytic Chronic infections
Iron deficiency,Thalessemia
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CLINICAL APPROACH TO AN ANEMIC CHILD1. Age2. Sex/ Family history3. Community4. Dietary history5. History of drug ingestion6. Infections and infestations7. Associated conditions –
hepatosplenomegaly, bleeding diasthesis, skeletal abnormality, facies
8. Features due to anemia- pica, changes in epithelia cells etc
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CLINICAL APPROACH TO CHILD WITH ANEMIA05/02/2023
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LABORATORY APPROACH Screening and confirmatory tests1. peripheral smear examination in case of
anemiaa) Sizeb) Shape (poikilocyte) – c) polychromasia – reticulocytosisd) Heinz bodies – G6PD, thalassemia chemical
injury etc.e) Howell Jolly bodies – (nuclear remnants)f) Parasite
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PS CTD
Changes in WBC – leukoerthroblastic picture, hypersegmented neutrophils
Changes in Platelets – 2- Blood indices –
MCV MCHMCHC RDW
3- Reticulocyte count – N -0.5-2%, & 2-6%Corrected RC = Pt RC X Pt hematocrit
Normal hematocrit
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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 anemiapost hemorrhagic, hemolytic anemia, renal and encocrinal disorders
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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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IRON DEFICIENCY ANEMIA
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INTRODUCTION Most common hematologic disease of
infancy and childhood.
Prevalence – 30% of the global population.
Deleterious health conditions-Work productivitySevere anemia and child mortalitySevere anemia and maternal mortality Iron deficiency anemia and child development.
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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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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
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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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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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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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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CLINICAL MANIFESTATIONS 05/02/2023
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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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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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INVESTIGATION Hb and CBC
Peripheral smear- anisocytosis, microcytes, pencil cells, hypochromia.
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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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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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Reticulocyte hemoglobin content
Molecular gentics of iron deficiency
Stainable iron in the bone marrow
Response to therapy –
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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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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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RESPONSE TO IRON THERAPYTime Response12-24 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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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 and3. Fortification of foods
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Compound % if elemental ironCarbonyl iron 100Ferric ammonium citrate 18Ferrous bisglycinate 20Ferrous fumarate 33Ferrous gluconate 12Ferrous sulphate 20Ferrous sulphate dry 30
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