National family health survey
(NFHS-III) in 2005-06 found that
the prevalence of anemia under 5
children approach about 70%.it is
highest in children between 6-35
months of age.
DR. VIJAY KR. SINGH(DNB PED)
UNDRE GUIDENCE OF
DR. T. K. MONDAL MD(PED)
M R BANGUR HOSPITAL
Decreased erythropoesis either due to deficiency
of nutrition or defect in erythipoesis
Increased blood loss.
Diminished red cell survival as a result of
immune disorder and chronic diseases.
Inadequate iron supply at birth like- prenatal or
maternal nutrition deficiency, prematurity, low
birth weight, multiple birth.
Inadequate absorption of iron-
Gluten induced entrepathy,
atrophic gastritis, post –
gasterectomy, presence of phytats
in diet and calcium, presence of
A. disorder of red cell production in which the
rate of red cell production is less than
1. marrow faillure
- Aplatic anemia( congenital and aquired)
2. Pure red cell aplasia
Diamond- Blackfan Syndrome
Transient erthroblastopenia of childhood
C. Bone marrow replacement
Chronic renal disesas
Chronic renal disease
Protein energy malnutrition
Hemoglobin mutant with decreased affinity of
Abnormalities in cytoplasmic maturation
Abnormalities in nuclear maturation
Thiamin respond megaloblastic anemia
hereditary abnormalities in folate
Iron deficiency anemia is the most
wide spread micronutrient deficiency
and affect nearly 1.5 billion people
Infant,pre school children,
adolescent, and growing children are
at greater risks.
According to NFHS-III in 2005-06,
the prevalence of anemia under -5
yrs of children is about 70%.
Normal infant have 75mg of iron
of per kg body weight.
Two third present in RBC.
The majority of body iron is in the
form of Hb with about 10% in iron
containing protien like myoglobin
green leafy vegetable
Bajra, dates, Nuts,
Meat and fish
Administration of Vitamin- C
increased the absorption of iron
A. Decreased iron store
Small for date baby
B. Decreased intake assimilation
Delayed intake of complementary feeding
Poor iron diet
Chronic diarrhoea/ infection
Gastero- intestinal surgery
C. Increased loss
Gastro intestinal bleeding
Hook worm infestation, trichuris
Diveticulutis, bleeding diathesis,
feto- femoral haemorrahagem, repeated
Recovery from mal nutrition
Mostly are asymptomatic.
Pallor is most important clinical sign but
usually not visible until Hb fall to 7-8gm/ dl.
Initial manifestation irritability, anorexia,
pallor, hyper dynamic circulation leads to
Shortness of breath, easy fatigability, exercise
intorelerance, heart failure.
Sign- koilonychias, glossittis, angular chellitis,
these are more common in long standing
RDW – Increased>19
Peripheral smear shows-
Hypochoromic microcytic red cell
with sustacial variation in cell
size, elliptocytic or cigar shaped
red cell are seen.
Study Iron deficiency
thalassemia Anemia of
Hemoglobin Decreased Decreased decreased
MCV Decreased Decreased Decreased-
RDW Increased Decreased Normal-
RBC Decreased Normal-
Serum ferritin Decreased Normal Increased
Increased Normal Dcreased
Reticulocyte Decreased Normal Normal -
Daily doses of 3-6 mg of elemental iron per kg of
body weight in two or three divided doses
Parental iron prepation is usually used only in
Parental iron sucrose and gluconoate complex have
a lower risk of serious reaction than dextran.
Doses of parental iron-2.3x body weight( 15-
patient Hb in gm/dl) +500 to 1000 mg, given in
Excessive intake of milk should be avoided
Repeat blood count after 4weeks
Hb begins to increased 0.1 to 0.4
gm/ dl per day.
Iron medication should be
continue for 8weeks after blood
value normalized to re-
establishment a response to
12-24 hrs Replacement of intracellular iron enzyme , subjective
improvement, decreased irritability, increased appetite
36- 48 hrs Initial bone marrow response, erythroid hyperplasia
48-72hrs Reticulocytisis, peaking at 5-7 days
4- 30 days Increased in Hb level
1- 3 months Repletion of store
Incorrect dose or administration.
Malabsorption of absorbed iron.
On going blood loss.
Concurrent vitamin B 12 deficiency or fIoate
Diagnosis other than iron deficiency like
Hb C and E disorder
Anemia of chronic diseases
lead poisoning, sickle cell anemia
Sideroblastic anemia result from
disorder of heme synthesis.
Characterized by microcytic, mixed
with normal RBC a picture of
dimorphic anemia with high RDW,
serum iron elevated and trasferrin
saturation increased. Elevated iron
deposited in mitochondria.
Megaloblastic anemia is characterized by
macrocytic red cells and erthroid precursor which
show nuclear dymaturity.
The common causes are Vitamin B12 and Folic
incidence of folate deficiency as 6.8% and vitamin
B12 32% and combined 20%.
Megaloblastic anemia affect all hem
poetic cell line resulting anemia,
thrombocytopenia, and leucopenia.
DNA synthesis impaired because of
lack of methytetrahydrofolate, vit B12
plays an important role as co factor
which is necessary for DNA synthesis.
Folate deficiency caused by
Trimithprine, azathiprine, phynatoin and other
anticonvulsent and increased requirement infancy,
hyperthyroidism, chronic hemolytic disease.
Vitamin B 12 deficiency causesd by
Intritrisic intestinal diseas
intrinsic factor deficiency
H. pylori infection
Glossitis, stomatitis, hyper pigmentation over skin
Enlarged liver and spleen in 30- 40% cases.
loss of position sense, vibration sensation,
memory loss, confusion, and neuron psychiatric
Hyper segmented neutrophil.
Bone marrow shows one or more cell
Bone marrow is cellular and nuclear –
Elevated lactate and billirubin.
Folate- 1-5 mg/day for 3-4 weeks
Vitamin B 12 500-1000micro gram for 2-3
weeks then 100-250 micro gram once in a
month to prevent recurrence.
Treatment with folic acid alone can produce
hematological response in vitamin B 12
deficiency but does not currect neurological
impairment caused by Vitamin B12
Difinition- A term infant have higher
hemoglobin and hematocrit and larger RBC than
older child and adult, within the 1st week of life a
progressive decline of Hb level begins then
persist for 6-8wks of life called physiological
anemia of infancy.
Causes – there is gradual , normal development
switch from Hb F to adult Hb after birth which is
capable of delivering of more oxygen to the
tissue.The increased in blood oxygen content
and delivery result in the down regulation of
erythropoietin production leading to suppression
Tratment- No therapy required
Hb may decreased to 8gm /dl at 4-8 weeks
of life in premature neonate with birth
weight less than 1.5 kg.
Factors which contributes development of
Reduced hematopoietic activity as evident
by decreased reticulocytes counts
Reduced red cell survival.
Treatment – recombinant human
erythropoietin with or without transfusion.
with adequate protein vitamin E, iron to
achieve full benefit of medication.
A plastic anemia is defined by as
presence of any two peripheral
blood criteria ANC(Absolute
neutrophil count) < 1500/mm
platelet count < 40,000/cumm.
Thrombocytopenia, with bleeeding in
skin, mucasal, GI tract, hematuria,
Neutropenia leads to fever, infection.
Anemia appears last with
breathlessness, puffiness of face,
edema of feet, congestive cardiac
Peripheral smear- normocytic
decreased ANC, Thrombocytopenia.
Coagulation parametre will be normal.
Bone marrow biopsy
hypocellular marrow with empty
spicule, increased fat space,
Curative-stem cell transplant
Criteria for stem cell transplant
1. Patient who are young
2. Severe a plastic anemia
3. Matched related sibling donor
Associated features Risk of malignancy
AR Absent thumb,absent radius,
ral and liver
Nail dustrophy, leukoplakia, Squamous cell
AD, AR Short stuture,congenital
anomalies , elevated Hb F,
Raised adenosine deaminase,
Diamond blackman syndrome is isolated
erythroid hypoplasia occurs in early child
hood and associated with congenital
anomalies like stabismus, webbed neck,
deformed thumb, bony abnormalities of
finger and thumb, double ureter,
Bone marrow shows profound erythroid
hypoplasia, macrocytosis. Inceased Hb F
Treatment-transfusion therapy, and
A rare disorder characterized by
diminised megakaryocytic tith
stem cell defect without
associated physical defect or
A variety of cells are abnormally sensitive
by complement, due to defect in
glycosylphosphatidylinositol anchor, which
bind protein to the cell membrane.
Chronic hemolytic is more common than
sleep- induced hemoglobinuria.
Diagnosis – molecular testing of CD-56
It is characterized by presence of
vacuoles in bone marrow precursor
cells along with sideroblastic anemia
with pancreatic exocrine