Anaemia in children
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Transcript of Anaemia in children
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