Anaemia in pregnancy

1. ANAEMIA IN PREGNANCY

2. PHYSIOLOGICAL CHANGES IN PREGNANCY
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. IRON ABSORPTION & TRANSPORT
 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 .

5. IRON TRANSPORT AND METABOLISM
 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.
 Most part of excess of iron is stored in
hepatocytes of liver and a little of it in RE
cells.

6. HAEMOPOESIS

7. REGULATORY FACTORS OF ERYTHROPOESIS
 Erythropoetin ----90 % produced by renal tubular
epithelium ., hypoxia or < P O2 level stimulates its
production. 10 % is produced in liver .
 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.

8. MATURATION OF RBC----
 It requires 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.

9. LIFE SPAN OF RBC AND ITS DESTRUCTION
 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).

10. ANAMIA IN PREGNANCY.
 Commonest medical disorder in pregnancy.
 20% of pregnant women are anaemic in developed
countries as compared to 40-75 % in developing
countries .
 It is responsible (directly / contributory factor ) for
significant high maternal and fetal mortality and
mortality throught out world , but more so in
developing nations.

11. WHO DEFINITION OF ANAEMIA IN PREGNANCY
 For diagnosis of anaemia in Pregnancy when
HB concentration is < 11 gm%) and a
haematocrit of < 0.33.
 Mild------------ 8 – 10 mg %
 Moderate ---- 5 –< 8 mg %
 Severe---------- < 5 mg %

12. RED BLOOD CELLS
 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.

15. TYPES OF ANAEMIA DURING PREGNANCY
1 . Hereditary causes
 Thalassaemias
 Sickle Cell Haemoglobinopathies
 Haemolytic anaemias
 other type of Haemgobinopathies.

16.  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 . Acquired hemolytic anemia.

17. IRON DEFICIENCY ANAEMIA (IDA)
 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.

18. CLINICAL FEATURES OF ANAEMIA IN PREGNANCY
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
standing
Hepatic –splenic enlargement .
Symptoms of congestive cardiac
failure

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

20. DIAGNOSIS OF IDA
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
Normochromic
Microcytic
Hypochromic
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

21. TREATMENT OF IDA
 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 .

22. PROPHYLAXIS----
 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.
 As hook worm infestation is common in some
countries, 400mg single dose Albendazole or
Mebendazole 100mg B.D. for 3days therapy is
recommended there.

23. TREATMENT OF IDA----ORAL IRON
 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 .

24.  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.

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

26. PARENTERAL THERAPY
 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.

27.  Iron Dextran – 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.

28. ANEMIA AND BLOOD TRANSFUSION --
 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.

29. FOLATE DEFICIENCY ANAEMIA ---
 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 .

30.  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.

31. FOLIC ACID DEFICIENCY ANAEMIA --
 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 .

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

33. TREATMENT
 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.

34. CYANOCOBALAMIN (VIT .B12 ) DEFICIENCY
 A uncommon 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 .
 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 .
 Parenteral Vit B12(cynocobalamin ) 250ug / month is
the treatment.

36. HAEMOGLOBINOPATHIES
 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 .

37. THALASSAEMIA
 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 .

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

39. THALASSAEMIA
 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 has normal Hb Or trait only pregnancy
can be continued and mange the anaemia by
blood transfusion as per need.

40. SICKLE CELL HAEMOGLOBINOPATHY
 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 .

41. SICKLE CELL HAEMOGLOBINOPATHY
 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

42. HEMOLYTIC ANAEMIA
 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.

43. SPHEROCYTOSIS
 RBC are small and sphere shaped , rather then
being biconcave disc.
 There cell membrane is also fragile .
 RBC destruction is faster then their production.
 Haemolytic anaemia develop.

44. APLASTIC ANAEMIA
 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.

45. KEY POINTS
 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