Approach to anemia and iron deficiency anemia

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

Transcript of Approach to anemia and iron deficiency anemia

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APPROACH TO ANEMIA AND IRON DEFICIENCY ANEMIADr Tushar JagzapeAssociate Professor,Pediatrics,AIIMS , Raipur

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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

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INTRODUCTIONIncidence – 71% in Urban children

84% in Rural children Common in period of rapid growth.

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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

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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%

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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

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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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