NUTRITIONAL ANEMIAS IN

CHILDREN
DR.M.DASARADHA RAMI REDDY
M.D.,D.C.H.,

PROF OF PEDIATRICS,
KIMS,NARKETPALLY

Overview
Definition
Nutrients

in hematopoesis
Prevalence
Common nutritional anemias
Iron deficiency anaemia (IDA)
Megaloblastic anemias

ANEMIA
What

is Nutritional Anemia:
Reduced Red blood cell mass due to
deficiency of nutrients required for
RBCs.

Nutrients required for RBC

production
Proteins
Fats
Vitamins
Trace

elements etc

Nutrients required for RBC

production

Proteins- all

essential amino acids are necessary;

methionine deficiency megaloblastic anemia
Vitamins - B12 and folic acid megaloblastic anemia
-C- Fe+++ to Fe++ & Releases Fe from stores.
-A- mobilises Fe from stores & improves
utilisation
-B6- macro/micro anemia,
-B2- BONE MARROW-hypoplasia--- Trace elements: iron,copper zinc
In PEM and other hematopoietic nutrient(s)
anemia on Fe- suppl alone will have poor
response.
5

Prevalence of nutritional anemia

ICMR 1999-2000-

11 states 19 districts 84.6%

(Hb <7.0 g/dl- 9.9% ).

90%

adolescents were also anemic Teoteja et al

2000.

>80%

< 3 yr children are anemic NFHS-II&

Agarwal et al.

NUTRITIONAL ANEMIAS IN CHILDREN

COMMON NUTRITIONAL ANEMIAS

DEFICIENCY OF
IRON
FOLIC ACID
VITAMIN B12

IRON DEFICIENCY ANEMIA ( I D A )

Iron

is not like gold that glitters or silver

that shines, however,it outshines both in
its biological importance
All adolescents across the country should
have at least 12 gm% Hb by 12 years of
age (12 by 12 initiative programme)

NUTRITIONAL ANEMIAS IN CHILDREN

IRON DEFICIENCY ANEMIA ( I D A )

MOST COMMON HEMATOLOGICAL DISEASE IN
INFANCY
MOST COMMON NUTRITIONAL ANEMIA IN
INFANCY
30% OF GLOBAL POPULATION SUFFERS FROM IT
IN INDIA IT IS 50%
IT AFFECTS CHILD DEVELOPMENT&BEHAVIOUR

Destribution of iron

Iron containing enzymes

NUTRITIONAL ANEMIAS IN CHILDREN-IDA

SOURCES OF IRON
ANIMAL-MEAT,LIVER,KIDNEY,EGG YOLK
VEG-PULSES,BEANS,GREEN VEGETABLES
PEAS,FRUITS.
HUMAN MILK-0.29-0.45mg/dl
COWS MILK- 0.01-0.38mg/dl

NUTRITIONAL ANEMIAS IN CHILDREN-IDA

IRON CONTENT OF NEW BORN-0.5g
IRON CONTENT OF ADULT - 5g
ABSORPTION OF DIETARY IRON-10%
DAILY REQUIREMENT
8-10mg
+ve BALANCE REQUIRES 1mg/day
IRON IS ABSORBED MORE FROM BREAST
MILK.

NUTRITIONAL ANEMIAS IN CHILDREN-IDA

DIETARY IRON IS IN FERRIC FORM
ABSORBED IN FERROUS FORM
GASTRIC SECRETIONS DISSOLVE IRON &FORM SOLUBLE
COMPLEXES WITH ASCORBIC ACID
SOLUBLE COMPLEXES REDUCED TO FERROUS FORM BY
FERRIC REDUCTASE &ABSORBED
IRON BINDS TO TRANSFERRIN IN PLASMA
TRANSFERRIN-IRON TRANSPORT PROTEIN
FERRITIN-STORAGE FORM OF IRON
IRON IS STORED IN R E SYSTEM AS FERRITIN.
IRON ALSO STORED IN B M AS HEMOSIDERIN
TRANSFERRIN RECEPTOR

Nutritional anemias in children-IDA

METABOLISM OF IRON

Nutritional anemias in children-IDA

Daily

iron cycle

NUTRITIONAL ANEMIAS IN CHILDREN-IDA

REGULATION OF IRON ABSORPTION
DIETARY FACTORS
Physico chemical form (ferrous form
better absorbed),
Other dietary constituents (phosphates, phytates,
calcium, tannic acid, etc.),
Iron dose
HOST FACTORS-Iron stores
OTHER FACTORS
Rate of erythropoiesis,
Physiological state
Gastric juice

STAGES OF IRON DEPLETION

Overload

Normal

Depleted
Stores

ID

IDA

Serum
Ferritin

Transferin
Satur.

Erythrocyte
Protoporph.

MCV

Hemoglobin

NUTRITIONAL ANEMIAS IN CHILDREN-IDA

CAUSES OF IRON DEFICIENCY ANEMIA

DIMINISHED INTAKE
DIMINISHED ABSORPTION
DEFECTIVE METABOLISM
CHRONIC BLOOD LOSS
DIMINISHED STORES
INCREASED DEMANDS

NUTRITIONAL ANEMIAS IN CHILDREN

DIMINISHED INTAKE
Not breast feeding,Cows milk feeding
Iron poor diet
DIMINISHED ABSORPTION
Malabsorption
High level of inhibitors
DEFECT IN METABOLISM
Idiopathic pulm. Hemosiderosis
Sideroblastic anemia
Congenital transferrin deficiency

NUTRITIONAL ANEMIAS IN CHILDREN

CHRONIC BLOOD LOSS

Occult bleeding (erosive gastritis, drug induced

Recurrent diarrhea)
Hookworm
Polyposis
Prolapse rectum
Portal hypertension
Dysentery
Meckels diverticulum
Hiatus hernia
Cephalhematoma

NUTRITIONAL ANEMIAS IN CHILDREN

DIMINISHED STORES
Preterm & small for date babies,Twins
Early cord clamping (100ml of blood),APH
Feto-fetal or feto-maternal transfusion
INCREASED DEMAND
Rapid catch up growth in preterm and SFD
Infancy & puberty

NUTRITIONAL ANEMIAS IN CHILDREN

CLINICAL FEATURES
Pallor,

pica, dull, irritable, poor appetite

Failure to thrive, easily fatigued
Frequent infections
Decreased attention span, poor school
performance, cognitive impairment
Malabsorption and protien loosing
enteropathy

NUTRITIONAL ANEMIAS IN CHILDREN

CLINICALFEATURES
Tongue

papillae are atrophied

Nails-flat, thin, brittle, spoon shaped
(koilonychia)
Splenomegaly in 15%
Severe cardiomegaly & CCF

NUTRITIONAL ANEMIAS IN CHILDREN

LAB DIAGNOSIS OF I D A

PBS
Low

Hemoglobin
Low Hematocrit
Low Mean Corpuscular Volume
Serum iron
Serum Ferritin <10ng/ml
Transferrin Saturation<15%
TIBC>350g/dl
Increased free erythrocyteprotoporphyrin

NUTRITIONAL ANEMIAS IN CHILDREN

LAB DIAGNOSIS OF I D A

Bonemarrow staining
Reticulocyte

hemoglobin content
Stool examination
Lead estimation

NUTRITIONAL ANEMIAS IN CHILDREN

DIFFERENTIAL DIAGNOSIS

-THALASSEMIA TRAIT-INCREASED HB A2 & FETALHB,

S.IRON,TIBC-NORMAL
RBC COUNT IS ELEVATED
RDW IS NORMAL(IDA-RDW^)

LEAD POISONING- ELEVATED BLOODLEAD,FEP &

URINARY COPROPORPHYRIN LEVELS

NUTRITIONAL ANEMIAS IN CHILDREN

Treat

THERAPY OF I D A

underlying cause
Oral iron therapy
Dietary measures
Activity restriction
Surgery

NUTRITIONAL ANEMIAS IN CHILDREN

THERAPY OF I D A
Oral iron

therapy

3-6mg/kg in 3 divided doses ( Hb rises by 0.4g/day)

For 6-8 wks after Hb is normal
Iron productsFerrous sulfate
Carbonyl iron(slow release)

NUTRITIONAL ANEMIAS IN CHILDREN

THERAPY OF I D A
Parental

iron therapy ( Iron in mg=wt in kg Hb

deficit in gm/dl4)
Products
Iron dextran complex
Ferric carboxy maltose
non dextran IV carboxymaltose

Indications for parenteral

therapy
Intolerance

to oral iron
Malabsorption
Ongoing blood loss where oral
replacement can not match iron loss

Reasons for non response

Poor

compliance
Associated B12/Folate deficiency
Interaction with drugs & diet
Hemolytic anemia
Malabsorption
Enteric coated iron preparations
Increasing on going blood loss.

NUTRITIONAL ANEMIAS IN CHILDREN

THERAPY OF I D A
Blood

transfusion rarely when Hb<4gm/dl, CCF,

severe infection with poor iron utilisation

NUTRITIONAL ANEMIAS IN CHILDREN

PREVENTION OF I D A
Breast

feeding and appropriate weaning diet

Iron rich food
Preterm and LBW babies-10-15 mg/day iron
Iron supplementation during puberty
Increase ascorbic acid

NUTRITIONAL ANEMIAS IN CHILDREN

PREVENTION OF I D A
Decrease

inhibitors
Salt fortification
Deworming
Foot wear use
Safe drinking water

NUTRITIONAL ANEMIAS IN CHILDREN

MEGALOBLASTIC ANEMIA

INEFFECTIVE ERYTHROPOESIS
DEFECTIVE SYNTHESIS OF DNA
INCREASED MCV
HYPERSEGMENTED NEUTROPHILS

NUTRITIONAL ANEMIAS IN CHILDREN

CAUSES OF MEGALOBLASTIC ANEMIA
FOLIC ACID DEFICIENCY
VITAMINB 12 DEFICIENCY
MALNUTRITION
INBORN ERRORS OF METABOLISM

NUTRITIONAL ANEMIAS IN CHILDREN

MEGALOBLASTIC ANEMIA

FOLIC ACID DEFICIENCY

VITAMINB 12 DEFICIENCY

NUTRITIONAL ANEMIAS IN CHILDREN

FOLIC ACID DEFICIENCY ANEMIA

SOURCES OF FOLIC ACID:

-Green vegetables,fruits,
-Non veg liver,kidney

NUTRITIONAL ANEMIAS IN CHILDREN

FOLIC ACID DEFICIENCY ANEMIA
CAUSES

INADEQUATE FOLATE INTAKE(GOATS MILK)

DECREASED FOLATE ABSORPTION(DRUGS)
DEFECTIVE FOLATE METABOLISMCongenital Dihydrofolate reductase deficiency
DRUG INDUCED
LAB DIAGNOSIS-P B S,RETIC COUNT, MCV >100fL
HYPER SEGMENTED NEUTROPHILS
SERUM & R B C FOLATE LEVELS
SERUM L D H
BM ERYTHROID HYPERPLASIA

NUTRITIONAL ANEMIAS IN CHILDREN

FOLIC ACID DEFICIENCY ANEMIA
CLINICAL FEATURES
WEAKNESS,FATIGUE,IRRITABILITY
PALLOR,GLOSSITIS,DIARRHOEA,
USUALLY ASSOCIATED WITH KWASHIORKAR AND
MARASMUS.
.

NUTRITIONAL ANEMIAS IN CHILDREN

THERAPY OF FOLIC ACID DEFICIENCY ANEMIA
If diagnosis is established
Folic acid 0.5mg-1.0mg/day oral/parenteral
If diagnosis is in doubt
Folic acid 0.1mg/day for 1wk as a dignostic test.
Doses >0.1mg/day can correct anemia of B 12
deficiency but may aggrevate neurological signs
DURATION OF THERAPY:
Folic acid 0.5mg-1.0mg/day for 3-4 wks
maintainance 0.2mg/day

NUTRITIONAL ANEMIAS IN CHILDREN

VIT B12 (COBALAMINE )DEFICIENCY
CAUSES MEGALOBLASTIC ANEMIA
HUMANS CAN NOT SYNTHESISE B12
MAIN SOURCE IS NON VEG FOOD

NUTRITIONAL ANEMIAS IN CHILDREN

VITAMIN B12(COBALAMINE) DEFICIENCY
METABOLISM OF B12
Ingestion- Cobalamine in Food
Stomach-Cobalamine combines with R Protein&IF
Duodenum-Pancreatic proteases break R protein
Distal ileum-Cobalamine with IF is absorbed.
Plasma-Cobalamine binds to transport protein,TC II.
In Cells- cobalamine enters cells by endocytosis
Cobalamine is converted to Methyl cobalamine&
Adenosyl cobalamine which are important in
DNA synthesis

NUTRITIONAL ANEMIAS IN CHILDREN

VIT B12(COBALAMINE) DEFICIENCY ANEMIA
CAUSES
Inadequate intake
Lack of Intrinsic Factor(I F )-congenital,juvenile
Impaired absorption
Absence of vit B12 Transport Protein.

NUTRITIONAL ANEMIAS IN CHILDREN

VIT B12(COBALAMINE) DEFICIENCY ANEMIA
CLINICAL FEATURES

WEAKNESS,FATIGUE,IRRITABILITY
FTT,DEVELOPMENTAL DELAY
PALLOR,GLOSSITIS,DIARRHOEA
SENSORY DEFICITS,NEURO PSYCHIATRIC CHANGES
ATAXIA,HYPOREFLEXIA,SEIZURES,BABINISKIS
RESPONSE
NEUROLOGICAL MANIFESTATIONS CAN OCCUR WITH
OUT HEMATOLOGICAL MANIFESTATIONS.

NUTRITIONAL ANEMIAS IN CHILDREN

VIT B12 DEFICIENCY ANEMIA

LAB DIAGNOSIS
Hematological manifestations of folate &B12
deficiency are similar
Macrocytes ,ovalocytes,hypersegmented neutrophils
Neutropenia,Thrombocytopenia
S.Vit B12 levels low
S.Methylmelonic acid,homocystein levels
S.Iron &folic acid normal,
Serum LDH
Urine Methylmelonic acid
Schilling test abnormal in pernicious anemia

NUTRITIONAL ANEMIAS IN CHILDREN

VIT B12 DEFICIENCY ANEMIA
SCHILLING TEST
Patient ingests radio active vitamin
After 2hrs pt receives 1mg of non radioactive vitamin
parenterally
Normally 30% of radioactive vitamin is excreted in urine in
24hrs
If radio active vitamin is <2% in urine it is abnormal
Test is abnormal even after therapy reversed the disease

NUTRITIONAL ANEMIAS IN CHILDREN

TREATMENT OF B12 DEFICIENCY ANEMIA
VIT B12- 1mg parenterally gives prompt response
If there is neurological involvement 1mg IM daily
for 2wks
Maitainance 1mg IM once in a month life long.

NUTRITIONAL ANEMIAS IN CHILDREN

TO SUM UP

NUTRITIONAL ANEMIAS ARE TREATABLE

CAN BE CONTROLLABLE
INTERVENTIONS ARE SIMPLE
INTERVENTIONS ARE AFFORDABLE
AFFORDABLE MEASURES ARE AVAILABLE

Thank you

NUTRITIONAL ANEMIAS IN CHILDREN

IRON ABSORPTION
SITE:DUODENUM& JEJUNUM

FERRITIN: IRON ABSORBED BY MUCOSAL CELLS

BINDS TO A PROTEIN CALLED APOFERRITIN
FORMS FERRITIN,(STORAGE FORM OF IRON)
IRON IS STORED IN R E SYSTEM AS FERRITIN.
IRON ALSO STORED IN B M AS HEMOSIDERIN
TRANSFERRIN-IRON COMBINED WITH IT IN PLASMA
TRANSFERRITIN RECEPTOR

NUTRITIONAL ANEMIAS IN CHILDREN

LAB DIAGNOSIS OF IDA

Low Hemoglobin

Low Hematocrit
Low Mean Corpuscular

Volume
Serum Ferritin <10ng/ml
Transferrin Saturation<15%
TIBC>350g/dl
Increased free erythrocyte
protoporphiryn

Iron fortified food.

Iron EDTA has been highly effective in

fortification trials with Egyptian flat breads,
curry powder in South Africa, fish sauce in
Thailand, and sugar in Guatemala.
In Grenada , flour used in commercial baking
is enriched with iron and B vitamins,.
Indian researchers have field tested with
success iron fortified salt.
Pasteurized milk (iron 15 mg/ l and Vit. C 100
mg/l.)-Stekel 1986

Availability of dietary iron by

cooking in cast iron utensils:

WHO 1992 prevalence of pregnancy anemia

report, records that lowest, rates of all the
subregions of the developing world were
observed in southern Africa, due to wide spread
use of iron cooking pots by indigenous people.
Agarwal et al (Lal et al IJMR-1973) had
demonstrated that cooking in cast iron utensils,
for boiling milk, cooking vegetables etc,
provided extra dietary iron. This available
dietary iron is well absorbed.

Iron physiology and

Dietary sources of Iron can be classified as
metabolism
food sources and fortified foods.
The

amount of Iron varies widely between

foods.
Iron exists in food under two
forms,
heme and non heme iron.
They are not only different in terms of their
sources, but also in terms of bioavailability.

Transfer of Iron to the

circulation and transport
Transferrin

is the major protein

responsible for transporting Iron in
the body.
Transferrin receptors, located on the
surface of nearly all cells in the body,
can bind two molecules of transferrin.
Transferrin saturation is important in
assessing ID.

 Tissues

with higher requirements of Iron

(erythroid precursors, placenta and liver)
contain higher transferrin receptors.
Once in tissues, Iron is stored as ferritin
and hemosiderin compounds, which are
present primarily in the liver, RE cells and
bone marrow.
The amount of ferritin in storage
compartment depends on Iron status which
ranges from depleted to replete iron status
Ferritin concentration expresses Body Iron
Stores when assessing ID.

Host related factors

Iron

stores and the amount of

iron to which intestinal cells
have been exposed constitute
the main factors regulating iron
absorption.

Laboratory Indices
LAB DIAGNOSIS

Low Hemoglobin

Low Hematocrit
Low Mean

Corpuscular Volume
Serum Ferritin <10ng/ml
Transferrin Saturation<15%
TIBC>350g/dl
Increased free erythrocyte
protoporphiryn

Treatment
Treat

THERAPY OF I D A

underlying cause
Oral iron therapy
3-6mg/kg

in 3 divided doses ( Hb rises by

0.4g/day)
Vit C, empty stomach or in between meals
For 6-8 wks after Hb is normal

Parental

iron therapy ( Iron in mg=wt in kg

Hb deficitin gm/dl4)
Blood transfusion rarely when Hb<4gm/dl,
CCF, severe infection with poor iron
utilisation

Response to treatment
Less

irritable & increased appetite

within 24 hrs
Bone marrow response by 48 hrs
Increased reti count by 3rd day
Increased Hb level by 2 months
Body iron store repletion

NUTRITIONAL ANEMIAS IN CHILDREN

NUTRIENTS IN RBC DEVELOPMENT

PROTEINS-(METHIONINE DEFICIENCY
LEADS TO DEFECTIVE DNA)
IRON
VITAMIN- B12
FOLIC ACID
VITAMIN C
VITAMIN A
VITAMIN B6
VITAMIN B2
OTHERS