Anaemia(IDA) in children

Dr.K.V.GiridharAssociate Prof. of Pediatrics

GMC. Ananthapuramu, A.P.,India.

• It is greek word• “Ana” = absent/ decresed• ‘emia’ = blood

Definition • Reduction of Hb con. Or Hematocrit

below the level of normal for that Age & Sex.

• Aprox. normal level of Hb in child hood – 11gm/dl

• Physiological anaemia of infancy.

WHO's Hb thresholds used to define anemia

Age or gender group Hb threshold (g/dl) Hb threshold (mmol/l)

Children (0.5–5.0 yrs) 11.0 6.8

Children (5–12 yrs) 11.5 7.1

Teens (12–15 yrs) 12.0 7.4

Women, non-pregnant (>15yrs) 12.0 7.4

Women, pregnant 11.0 6.8

Men (>15yrs) 13.0 8.1

classification of Anaemia

Anemia

Etiological

Morphological

Patho physiologi

calseverity

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Etiological classification of Anaemia

Anaemia

Decreased production

IDABone marrow suppression

Increased loss

Haemorrhage

Increased destruction

Clinical importance

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A)Aetiological classification:(Classification according to cause) 1. Anemia due to blood loss: a. Acute post hemorrhagic: It occurs due to any accident, which cause large amount of blood loss. Anemia is normocytic normochromic anemia b. Chronic post hemorrhagic: When small amount of blood is lost continuously from our body.E.g. in Hookworm infestation, chronic duodenal ulcer, bleed piles Anemia is initially normochromic normocytic but later changes to Hypochromic microcytic anemia.

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2.Anemia due to impaired red cell formation: a. due to disturbance of bone marrow function due to deficiency of factors necessary for erythropoiesis I.Iron deficiency anemia II.Megaloblastic anemia

b.due to disturbance of bone marrow function not due to deficiency of factor required for erythropoiesis 1.Anemia associated with chronic infection like renal failure, liver disease, disseminated malignancy

2. Bone marrow infiltration 3. Aplastic anemia

4. Anemia associated with myxedema,Hypopituitarism

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3.Anemia caused by excessive red

cell destruction: (Hemolytic anemias)

i.Intracorpuscular causes - production of Hb

(Thalassemia) - abnormal production of Hb

(hemoglobinopathies) – sickle cell anemia.

ii. extracorpuscular causes mechanical, antibodies X RBCs

etc.

Morphological classification

Size&color of RBCs

Normocytic normochro

mic

Microcytic hypochro

mic

Macrocytic anemia

Laboratory importance

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B Morphological classification:Based on characteristics of red cell as determined by blood examination (MCV, MCH, MCHC)

1. Normocytic normochromic anemia: Here MCV, MCH, MCHC are normal.E.g. aplastic anemia, acute post hemorrhagic anemia.2. Microcytic hypochromic anemia:

MCV: DecreasedMCHC: DecreasedMCH: DecreasedE.g. iron deficiency anemia

3. Macrocytic anemia: MCV: Raised. E.g. megaloblastic anemia

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Patho-Physiological

Increased demand

Decreased

production

Increased loss

• C. Patho physiological classification(how anaemia occurs)

• i. Increased demand. eg. infancy and childhood. Reproductive age and pregnacy in female.

• iii. Decrease production.• iii. Increased loss

SeverityWHO

Moderate7-10.9 g/dl

Severe4-6.9 g/dl

Very severe

<4 g/dl

-The primary function is oxygen transport.-Average total body iron content 3.5-4 g.-Approximately 2/3 found in hemoglobin, -Iron is also stored in RE cells (BM, Spleen and liver) as hemosiderin and ferratin.-Also iron found in myglobin and myeloperoxidase and in certain electron transfer.-Iron is more stable in ferric state (Fe+++) than in ferrous state (Fe++).

Normal iron metabolism:

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Distribution of iron in body

1. 65% in the form of Hb 2. 4% in the form of myoglobin in muscle 3. 1% in various heme compounds that promote intracellular oxidation (cytochrome, catalase, and peroxidase) 4. 0.1% in combination form with protein transferrin in blood plasma 5. 30% is stored mainly in R.E. system and liver cell as ferritin

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Forms of ironA) Hemoglobin ironB) Plasma (transport) iron: Those bound

with transferrinC) Tissue iron:

a. Available iron: In the form of ferritin and hemosiderin

b. Non-available iron:In the form ofmyoglobin.

In enzymes of cellular respiration Iron present as a constituent of cell

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Sources of iron: Meat, liver, egg yolk, peas, beans, lentils & green leafy vegetables.

Daily requirement(RDA): Male: 0.5-1 mgFemale during reproductive life : 1.5-2 mgPregnant women: 1.5-2.5 mg

Children : 0.5 mg/day

Daily dietary requirement:Male: 5-10 mgFemale: 15-20 mg

Children : 5-10 mgPregnant women = 20-30 mg

Only 10% of dietary iron is absorbed from gut, so dietary requirement is greater than body requirement

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Daily lossMale: 0.5-1 mg

Menstruating female: 1.5-2 mg

Absorption of iron: Iron absorption occurs mainly in duodenum and proximal jejunum.

 Form of absorption: Ferrous (Fe++)

(Iron found in food is in ferric form, so all ferric iron must be converted to ferrous iron for absorption in GIT)

Mechanism of absorption:Active transport (pinocytosis)

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clinical features of IDA

Symptoms • Easy fatigability• SOB• Lethargy • Drowsy • Dizziness • Head ache• De. Alertness • Palpitation • Pica

Signs • Pallor • Angular cheilosis• Beefy tongue• Koilonychia • Tachycardia • RD • CCF• Pharyngeal webs

Pallor

Koilonychia

Angular chelosis& tongue changes

Laboratory diagnosis:•Red cell indices: Low Hb conc. MCV, MCH, MCHC* •Blood film: Hypochromic microcytic Picture. Occasional Target cells. Pencil shaped poikilocytes. Normal reticulocyte count.•Bone marrow iron: Normal to hypercellular. RBC precursors are increased in number. Iron stain negative.•Chemical testing on serum: Serum iron : Decreased Transferrin/TIBC : Normal to High Serum ferritin : Decreased (Very low)

Hypochromic Microcytic picture (IDA)

-ve BM Iron Stain +ve

Labo. Approach (work-up)

M: Hb <13.5 Hct <41F:Hb <12 Hct <36 : Child ; Hb <11

[check MCV]

MCV <80 = microcytic• Fe deficiency• thalassemia• anemia of chronic disease• sideroblastic anemia

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MCV >100 = macrocytic• megaloblastic anemia• VitB12 deficiency• folate deficiency

• alcoholic liver disease

MCV 80-100 = normocytic

[chech reticulocyte count]

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low reticulocyte:- marrow failure - leukemia/metastasis- aplastic anemia - renal failure- Myelofibrosis - anemia of chronic disease

high reticulocyte:- sickle cell anemia - autoimmune

hemolytic anemia- G6PD deficiency - hereditary

spherocytosis- paroxysmal nocturnal hemoglobiuria

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Treatment Rx of ID anaemia

Supportive

Nutritional

O2, rest

Vit.c, Folate

Therapeutic

Elemental Iron

oral

parenteral

Blood transfusion

PCV

Whole blood

Complications of IDA

• Feeding problems• Delay in growth & Developement• Low IQ• Decreased scholastic performance• Rarely CCF *(if untreated death)

Prevention of IDA

• Promotion of exclusive breast feeding• Provision of iron rich foods (green

leafy veg. Red meat)• Nutritional anaemia Control

programme in children • Iron def. Anamia Control programme

for adolescent girls• Hook worm control programme

(Albendazole)

Thank you