This document discusses iron deficiency anemia in pregnancy. It notes that iron deficiency is the most common type of anemia globally, especially in developing countries. The document outlines the iron requirements and recommendations for treatment of iron deficiency anemia during pregnancy, including oral iron supplementation and parenteral iron therapy for more severe cases.

1. Prof. M.C.Bansal.
MBBS., MD. MICOG. FICOG.
Founder Principal And Controller
Jhalawar Medical college & Hospital Jhalwar.
Ex Principal & controller MGMC & Hospital
Sitapura ,Jaipur.

2.  Commonest medical disorder in pregnancy.
 18-20 pregnant women are anaemic in developed
countries as compared to 40-75 % in developing
countries .
 Itis responsible(directly / contributory factor )
for significant high maternal and fetal mortality
and mortality throught out world , but more so in
developing nations.

3.  For diagnosis of anaemia in Pregnancy when HB
concentration is < 11 gm% ( 7.45mmol/ L)and a
haematocrit of < 0.33.
 Mild------------ 8 – 10 mg %
 Moderate ---- 5 –< 8 mg %
 Severe---------- < 5 mg %
During Pregnancy there is increase in total blood volume
(1500 ml = 30 - 40%), plasma volume(250 ml = 40-50 %) as
well as the EBC volume (350ml = 20 -30 % ) also ,
But increment in plasma volume is more then the
increased total hemoglobin(15-20 % ).
Hence there is dilution of blood, resulting in physiological
anaemia( upper limit for normal / 100% Hb level in
pregnancy is brought down to 11gm % ) .

4. Nutrients Sources
Iron Haem Iron :Animal blood , flesh ,
viscera ( live Kidney , red meat ,
poultry and fish ( including muscles )
Non Harem Iron : green leafy
vegetables, cereals , seeds ,
Vegetables ( peas , backed beans )
roots and tubes , japery , Cooking in
iron vessels < urinal , Dates etc .
Folic Acid Green Vegetables ( palak, Maithy ,
bathali , Broccoli ) Fruits ,
Germinate wheat , Liver and Kidney.
Cyanocobalamin ( Vit B12 ) Meat , fish , eggs , milk
Ascorbic Acid ( vit. C ) Citrus fruits , Amala ( indian
gooseberry )
Other Vit,B Green leafy vegetables and fruits

5.  Iron is a critical element in the function of cells,
 Body should protect itself from ill effect of
excessive iron as it is highly toxic ,as it
generates free radicals such as singlet O2 / OH +
 Major role of iron (ferrous form ) is to carry O2
as part of hemoglobin . O2 is also bound by
myoglobin An iron compound present in muscles.
 Iron is a critical element of iron containing
enzymes including cytochrome system in
mitochondria.

6. iron content in mg.
Adult male Adult Female
80 Kg 60 Kg
Hb(65%) 2500 1700
Myoglobin (4%) & 500 300
Enzymes
Transferretin iron 3 3
(0.1%)
Iron Stores 600- 1000 0- 500
(15-30%)

7.  Ingested Iron- ferric form is changed to Ferrous form
by gastric HCl acid ,.
 It reaches in duodenum .
 Liver secretes Appoferrin in bile .
 Appoferrin combines with ferrous ion in duodenum
to form Transferrin.
 Transferrin attach to receptors present on intestinal
mucosa .
 Transferrin get absorbed in intestinal mucosa by
pinocytosis .
 Then transferrin is released in plasma to plasma
transferrin.
 Transferrin is circulated to tissue –the
loosely bound iron is released to tissue where
it is needed.

8.  Most part of excess of iron is stored in
hepatocytes of liver and a little of it in RE
cells.
 The unique characteristic of transferrin is
that it bounds strongly to the receptors
present on the cell membrane of
erythroblasts present in bone marrow.
 Endocytes in erythroblasts ingest the
bound form of iron .
 Apoferrin directly delivers iron molecule to
mitochondria where heam chain is
synthesized.

11.  Shape & Size –RBC are biconcave disc with 7.5 um in
diameter and 2.5 um in thickness at periphery but <
1um at center.
 Concentration in blood ---
5.2 mill/ cmm in man.
4.7 – 5.0 mill / cmm in female.
Hb Content in RBC ----RBC are able to concentrate Hb
in it cellular fluid up to 34 gm / ml of RBC.
Hb concentration in whole blood ---
14-15 gm % / ml in man
13.5 -14 gm % /ml in female.
Each Gm of HB is able to combine with 1.3ml of O2
., there by 100 ml of blood with normal Hb content
can absorb 20 ml and 19 ml of O2 in man and female
respectively.

12.  Erythropoesis starts in embryonic life in yolk sac
from pluripotent stem cells the original
pluripotent haemopoetic stem cells.
 In later foetal life it occurs mainly in red cells in
liver spleen and bone marrow.
 In neonatal life and child hood it occurs in bone
marrow of all the bones and liver.
 In adults all types of blood cell production occur
in bone marrow present in membranous bones
e.g. vertebra, sternum , ribs and iliac crest and
proximal ends of long bones.
 Pluripotent stem cells differentiate in to pro -
erythroblasts—the parent cell of RBC.
 Growth inducers and differentiation inducers
produced locally in bone marrow play a major
role in production of RBC and other cells.

15.  Erythropoetin ----90 % produced by renal tubular
epithelium ., hypoxia or < P O2 level stimulates
its production. 10 % is produced in liver .
 Nore epinephrin, epinephrin and PGS accentuate
development maturation of RBC after the pro-
erythroblast(from haemopoetic stem cells )
stage of production which takes about 5 days
and is under growth inducers in bone marrow.
 Low tissue O2 concentration ---as in high
altitudes, chronic blood loss , cardiac failure and
chronic lung disease etc.
 Increased demand for o2 carrying capacity –as in
pregnancy.

17.  Itrequires vit B 12 and Folic acid ----
Vit. B12 and Folic Acid are accential for
production of DNA .
Thyomidine Triphosphate is an important
building block Of DNA.
The deficiency of Vit B12 and Folic acid
leads to maturation failure of RBC , resulting
in megaloblast production.
These immature cells when appear in blood
circulation, serve no purpose of O2
transportation as efficiently as mature RBC.
Their life span is also small hence person
develops anaemia.

18.  Synthesis of Hb starts in proerythroblasts and
continues even in reticulocyte stage.
 First Succinyl –CoA is formed in Krebs
metabolic cycle . It combines with a
molecule of glycine to form Pyrole molecule
.
 4 molecules of Pyrole combine to form
Protoporphyrrin IX .
 Protoporphirrin IX combines with Ferrous
molecule to form Heam .
 Haem combines with Globin and Hemoglobin
chains (alpha & beta ) are produced.

19.  Depending upon presence or absence of amino
acid combination in poly peptide part of Globing
,. There are different types of Hob chains---like
alpha, beta , gama and delta.
 Adult Hb is Hb A and has 4 chains 2 alpha & 2
beta chains.
 Each HB chain has a Heam prosthetic group
containing an Iron ion.
 One HB molecule has 4 Heam chains and 4 iron
ions capable of absorbing 8 atoms of Oxygen.
4F+8o = 4 FO2(4 molecules of Ferrous
Oxide contain 4 molecules of iron and 4
molecules / 8 atoms of oxygen )

22.  Mature RBC circulate and remain alive
( active ) for 120 days .
 RBC face bear and tear in circulation and get
aged when they are engulfed by macrocyte
macrophages which dissociate iron from
haem .
 This iron is mainly stored in ferritin pool for
Hb production .
 Rest heam is denaturized in liver as bilrubin.
 Daily loss of Iron-0.6 mg iron is lost in
feces by male ,. But iron loss is more in
menstruating females (1.3 mg).

23.  1 . Hereditary causes Thalassaemias , Sickle Cell
Haemoglobinopathies , Haemolytic anaemias , other type of
Haemgobinopathies.
 2 .Acquired Causes 
A . Nutritional---Iron deficiency anaemia ( microcytic
hypocromic anaaemia , Folate deficiency anaemia (
megaloblastic anaemia ) , Vit B 12 Deficiency anaemia (
Megaloblastic anaemia )
B . Anaemia due to bone marrow failure ( aplstic / hypo
plastic anaemia ).
C . Anaemia secondary to inflammation , chronic disease ,
malignancy.
D . Anemia due to acute / chronic blood loss.
E . Acquire hemolytic anemia.
Note Iron Deficiency anemia is most common in developing
countries like ours

24.  This Is Most Common Type Of Anaemia.
 Hematologicaly described as Microcytic
Hypochromic Anaemia .
 More common in developing countries owing
to Low Dietary Intake Of Iron , Chronic
Intestinal Diseases Like Amoebiasis, Sprue,
Diarrhoea, Parasitic Infestation (Hook Worm)
Malaria , Schistosomiasis , Phytates In
Diet,chronic Blood Loss ( Menorrhagia , Piles,
Fissure In Ano ---Apathy To Take Treatment)
Too many and too frequent pregnancies and
plural pregnancy.

25. Symptoms Signs
Weakness Pallor .
Lassitude , tiredness , exhaustion Glossitis .
Indigestion Stomatitis .
Loss of appetite Oedema
Palpitation Hypoproteinaemia .
Breathlessness Soft systolic murmur in mitral area
due to hyperdynamic circulation
Giddiness / dizziness Fine crepitations at lung bases.
Swelling feet eye lids ( peripheral ) Pale nails . Platynaechoea .
Koilonaechia
Generalized anasarca. Tenderness in sternum .
Blackouts in front of eyes on sudden Hepatic –splenic enlargement .
standing
Symptoms of congestive cardiac
failure

26. Maternal Foetal
Weakness Preterm baby
Lack of energy Small for gestation
Fatigue Increased perinatal morbidity and
PET mortality
Poor work performance Iron deficiency
Palpitation Cognitive and affective dysfunction in
tachycardia the infant
Even mild bleeding in APH or PPH can Increased incidence of diabetes and
endanger the life cardiac disease in later life
Breathlessness
Increase cardiac output
Cardiac decomposition
Cardiac failure
Increased incidence of preterm labour
Sepsis

27. Characteristics Calculation Normal Range IDA
Hb gm % Sahli’s method 11-15 < 11
Mean corpuscular volume(MCV) PCV/RBC 75-96 <75
Mean corpuscular HB Hb /RBC 27-33 <27
Mean corpuscular Hb Conc. (g/dl) HB / PCV 32-35 <32
PBF(peripheral Blood Film ) Normocytic Microcytic
Normochromic Hypochrom
Serum Iron (ug/dl) 60 -120 < 60
Total iron binding capacity (ug/dl ) 300- 400 >350
Transferrin Saturation < 15%
Serum Ferritin (mcg / dl ) 13-27 <12
Free erythrocyte protophyrin (ug/ml) <35 >50
Serum Transferrin Receptors increased

28.  In average pregnancy , iron the requirement are :
Basal iron –280mg.
Expansion of Red Cell Mass –570 mg .
Fetal transfer ----200-350 mg.
placental---------- 50 -150mg.
blood loss at Delivery ---100-250 mg.
After deducting iron conserved by amenorrhoea (
240-480mg. ) , an additional 500-600mg .
Of iron is required in pregnancy . if she is chronically
anaemic then her iron stores are also depleted.,
hence 500mg more elemental iron is to be
prescribed.
There by total iron requirement will be 1000 mg .

29.  Extra iron requirement in pregnancy can be met with
balanced diet rich in iron containing food . Avoid food
containing Phytates , tannins (tea –coffee)known inhibitors
of iron absorption
 4-6mg elemental iron if absorbed / day during 2nd and 3rd
trimester ( over period of 1oo days ). Average daily
requirement of absorbed iron is 4m., beng2.5 mg/day in
early 1/2 , 5.5mg/day during 20- 32 weeks and 6-8mg /
day 1fter 32 weeks onwards of gestational period.
 Indian Government has recommended to prescribe
Tab Ferrous sulfate 100mg + 500ug Folic acid /
day for 100 days .
 As hook worm infestation is common , 400mg
single dose Albendazole or Mebendazole 100mg
B.D. for 3days therapy is also recommended.

30.  1. When anaemia is of mild to moderate degree and there
is plenty of time (> 30days) before EDD., oral iron therapy
with 200 mg elemental iron with 5mg Folic acid / day will
improve the Hb by 0.8 gm in a week . Reticulocyte count
start to increase with in 10 days after starting oral iron
therapy .
 Side effects (10-40% cases ) will develop mainly related to
GIT such as , nausea , vomiting , epigastric burning ,
constipation abdominal cramps and diarrhoea.
 There is no scientific evidence that any particular brand is
better .
 Slow release preparations are associated with less side
effect , but manly due to slow / decreased iron absorption
. Taking iron with ascorbic acid will decrease the GIT side
effects.
 Those who can not tolerate oral iron , carbonyl iron can be
started.
 There is no advantage in using parenteral iron over oral
iron , if oral iron is tolerated and there is plenty of time is
available.

31. IRON ELEMENTAL IRON
DOSE in mg
PREPARATION CONTENT (mg%)
Ferrous Fumerate 30 200
Ferrous Gluconate 11 550
Ferrous Sulphate 20 300

32. In moderate anemic , pregnancy near term ( 32-
34 weeks) , or oral iron is not tolerated ----
parenteral Iron therapy should be considered .
 total Iron Dose calculation 
Elemental iron (mg) = Normal HB – Pt’s HB
(gm%) x pt’s weight
in KG x 2,2 + 1000
Preparations 
Iron Sorbitol Injection– given deep IM after
sensitivity test –rapid absorption owing to
molecular wt., associated with pain and skin
discoloration at the site of injection .Total
calculated dose is given over 2 weeks of duration.

33.  IronDextran – can be given IM / IV route
after sensitivity test . It has minimal side
effects ,as it is highly fractionated low
molecular salt .
 Iron
Sucrose – can be given as single /
repeat dose in Iv drip.
Parenteral therapy will take 4-6 weeks to
reach their optimal effect.

34.  When Hb is < 5gm % and or pt is near term
and obstetrical haemorrhage .
 Digitilisation and Lasix therapy may be given
to control CHF or to prevent its
precipitation.
 PCV transfusion , if available is preferred
than Whole Blood .
 Recombinant Erythropietin can be used
along with parenteral iron therapy to the
patients having chronic renal disease
complicating pregnancy and to non
responders to oral / parenteral iron therapy.

35.  Folic acid is needed in higher doses during
pregnancy because of the increased cell
replication , taking place in fetus , uterus and
bone marrow.
 800 ug is required / day , but pre existing
deficiency is common especially in developing
countries . It is mainly due to inadequate diet /
intestinal malabsorption( sprue ) syndrome .
 More common in twin pregnancy , multigravida ,
hook worm infestation , GIT diseases , bleeding
piles , Haemolytic conditions , malaria and other
infections .
 Anti folate medications like anti epileptics , anti
cancer .
 Combined iron and folic acid deficiency anemia
is common in developing countries.

36. Symptoms 
Asymptomatic , loss of appetite, vomiting ,
diarrhoea, unwell with unexplained fever
Signs
Pallor Bleeding points on skin , Enlarged
spleen and liver and neuropathy.
Maternal complications  PIH, Abruptio placenta
.
fetal complications  Folate deficiency in
mother can cause fetal neural tube defects ,
abortion , IUGR, premature / small for date
fetus and poor folate level in newborn .

37. Characteristics Normal range Folic acid deficiency
Hb 11-15gm% <11 gm%
MCV 75-96 > 96
Mean corpuscular HB 27 - 33 33
Mean corpuscular HB 32-35 Normal
Conc.
PBF Normocytic Megalobastic , neutropenia ,
Normochromic thrombocytopenia,
hypersegmentation of
neutrophills
Serum Folate >3 <3
Red cell Folate >150 ng / ml < 150
Serum Iron 60-120 ug/dl Normal
Serum lactate Increased
dehydogenase
HomoCysteine Increased

38.  WHO recommends 800ug / day in
pregnancy and 600ug / day during lactation
period .
 To meet this need pregnant and lactating
women should be encouraged to eat more
green leafy vegetables ( palak , maithi ,
baithali , brocoli ) and offal ( liver and
kidneys .
 Treatment for patient with Folic acid
deficiency anaemia should take 5mg folic
acid / day for > 4 weeks .
 Response is observed by fall in LDH level in
3-4 days and increase in reticulocyte count
in 5-8 days.

39.  A rare cause of anaemia in pregnancy . , as daily
requirement of 3ug is easily met with a normal
diet .
 Pernicious anaemia due to absence of intrinsic
factor , resulting in decrease absorption of Vit
B12 is rare in pregnancy ., as it usually causes
infertility.
 Clinical findings are same as in folic deficiency .
 Vit B12 level is lower in the blood ( < 90ug / L)
Deoxyuridine test can differentiate in two .
 Parenteral Vit B12(cynocobalamin ) 250ug /
month is the treatment.
 Gastric mucosal atrophy following long term use
of H2 inhibitor and Proton pump inhibiting anta
acid will result in deficiency of intrinsic factor
and decreased absorption of Vit B12 .

41.  Each molecule of normal Hb is composed of
4 subunits , with a single heam group and 4
species specific globin chains .
2 pairs of globin chains ( 2 alpha & 2 Beta
chains ) are attached to the Pyrole rings to
make normal Hb . The integrity of the Heam
moety and amino acid sequence of globin
chain determine the structure of the globin
chain and interaction between the 4 sub
units of the Hb .

42.  Characterized by impaired of one or more of
globin chains .
 ALPHA Thalassaemia when alpha chains are
impaired . If only one alpha chain is impaired the
it is called Alpha Thalassaemia Trait.
 Beta thalassaemia When both Beta chains are
impaired. Beta Thalassaemia Trait if only one
Beta chain is impaired.
 Children With Beta Talassaemia usually die
before reaching reproductive age . Repeated
blood transfusion and Iron chelating therapy
some women remain alive , get married and
become pregnant. These women suffer from
chronic anaemia which need to be differentiated
from IDA., by Blood indices and Hb F and HbA 2
Levels .

43. Characteristics Normal Range IDA Thalassaemia
MCV 75-96 Reduced Very Reduced
Mean 27-23 Reduced Very Reduced
Corpuscular Hb
Mean 32 -35 Reduced Normal
Corpuscular Hb
Conc.
Fetal HB (HbF) <2% Normal Raised
HbA2 2-3% Normal Raised
Red cell width high normal

44.  If mother has Thalassaemia Trait , husband
should be investigated for Trait .If both
partners are positive for trait , prenatal
diagnosis for foetal is indicated .
 There is 1: 4 chances of fetus being
Thallassaemia major .
 Therapeutic termination of pregnancy is
indicted in such situation .
 If foetus is has normal Hb Or Trait only
Pregnancy can be continued and mange the
anaemia by blood transfusion as per need.

45.  O.1- 1.0 % in west African and American
blacks .
 RBC have abnormal HB called HbS, having
faulty Beta chains in Hb, results from a single
Beta chain substitution of glutamic acid by
Valine at colon 6 of Beta globin chain .
 When HbS is exposed to low O2 tension ,Hb
precipitates in long crystals , cell become
elongated and sickle shape . Red cell
membrane changes make these abnormal
shaped cells more fragile –life spine reduces
resulting in anaemia .

46.  It may have serious implications in pregnancy
and women may develop Sickle cell crisis.
 Patient frequently experience vicious circulation
events as progressive low O2 tension develops.
 Sickle cell crisis is an emergency with infarction
in various organs due to sequestration of sickle
cells , causing severe pain more so in long bones.
 It can happen any time in pregnancy , labour and
puerperium .
 Low Po2 in general anaesthesia can worsen the
crisis
 Treatment is by Iv hydration , O2 administration
and PCV transfusion.
 Prenatal diagnosis is indicate in sickle cell Trait
women with sickle cell trait husband , with
advice of MTP of an affected pregnancy

47.  Different types abnormalities in RBC
( acquired or hereditary) Make the cells more
fragile , hence rupture more easily and
frequently as they pass through capillary
circulation specially through spleen .
 RBC destruction is faster then their
production leading to chronic anaemia.
 Patient also develops pre hepatic (hemolytic)
Jaundice .
 Anaemia and Jaundice put a combined
burden over the pregnant women and hence
they carry high maternal as well as fetal
morbidity and mortality.

48.  RBCare small and sphere shaped , rather
then being biconcave disc.
 There cell membrane is also fragile .
 RBCdestruction is faster then their
production.
 Haemolytic anaemia develop.

49.  Bone marrow aplasia / hypoplasia means
arrest of production of all blood elements
like RBC, WBC and platelets
 PBF shows Pancytopenia .
 It can develop following bone marrow
function depression by radiations ,
chemotherapy , industrial chemicals , drugs
and viral infections .
 Repeated Whole blood transfusion ,
prednisolon , erythropoietin , nutrients ,
bone marrow transplantation Pluripotent
stem cell therapy is indicated.

50.  Anaemias specially nutritional deficiency , are
very common in pregnancy and are major health
problem , being more common in developing
countries .
 Most significant cause (direct & indirect ) of
maternal and perinatal mortality and morbidity.
 Iron deficiency anaemia continues to be the
commonest anaemia during pregnancy , owing to
poor dietary habits , can be treated by oral or
parenteral iron therapy .
 Folic acid deficiency anaemia is associated with
fetal neural tube defects can be easily
prevented by folic acid supplementation
 Thalassaemia and sickle cell anaemia are seen in
certain geographic areas , and are associated
with significant morbidity