anemia and pregnancy

1. ANEMIA AND
PREGNANCY
Supervised By:
Dr.Sausan
Presented to you By:
Shams Kareem
Rose Razzaq
Mohammed Tawffeq
Mohammed Haroon

2. ANAMIA IN PREGNANCY.
 Commonest medical disorder in pregnancy.
 18-20 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.

3. WHO DEFINITION OF ANAEMIA IN PREGNANCY
 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 %

4. WHY DOSE IT OCCUER ?! 
(PHYSIOLOGY)
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 % ) .

5. SOURCES OF VARIOUS NUTRIENT REQUIRED FOR
ERYTHROPOESIS
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

7. TYPES OF ANAEMIA DURING PREGNANCY
 Physiological anemia
 Pathological anemia icluding :
 1 . Hereditary causes
 Thalassaemias ,
 Sickle Cell Haemoglobinopathies ,
 Haemolytic anaemias ,
 other type of Haemgobinopathies.

8.  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

9. 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

10. 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

11. HOW ANEMIA IS DIAGNOSED?

12. BY EXAMINATION :-

13. IRON
 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.

14. IRON DEFICIENCY ANAEMIA (IDA)
This Is Most Common Type Of Anaemia.
 Hematologicaly described as Microcytic
Hypochromic Anaemia .
 More common in developing countries

15. Causes can include :
. Low Dietary Intake Of Iron ,
.Chronic Intestinal Disease Like
Amoebiasis, Sprue, Diarrhoea,
Parasitic Infestation (Hook Worm)
.Malaria ,
. Schistosomiasis ,
.Phytates In Diet,
.chronic Blood Loss (Menorrhagia ,
Piles, Fissure In Ano )

16. 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
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

17. 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 .

18. 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 ).

19. TREATMENT OF IDA----ORAL IRON
 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.

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

21. ORAL IRON THERAPY :-
 For women presents in mid trimester or early third
trimester
 For treatment more than 180 mg of elemental iron/day is
required
 To minimize side effects, start with low dose
 Treatment is continued till blood picture becomes normal,
thereafter maintenance of one tablet daily for 3 months to
replenish iron stores

22. SIGNS
OF RESPONSE TO THERAPY
 Sense of well being
 Improved outlook of patient
 Increased appetite
 ↑ haemoglobin, haematocrit, reticulocytosis within 5-10
days
If no significant clinical or haematological improvement
within 3 weeks, diagnostic re-evaluation is needed.

23. SIGNS OF RESPONSE TO THERAPY (CONTD.)
 RATE OF IMPROVEMENT:
After a lapse of few days haemoglobin concentration is
expected to rise at a rate of 0.7 g/dl/week.
 CAUSES OF FAILURE OF ORAL THERAPY
 Incorrect diagnosis
 Malabsorption syndrome
 Presence of chronic infection
 Continuous loss of iron
 Poor patient compliance
 Concomitant folate deficiency.

24. TREATMENT OF IDA --- 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.

25. PAENTERAL IRON THERAPY ----
 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.

27. ANEMIA AND BLOOD TRANSFUSION --
 When Hb is < 5gm % and or pt is near term and
obstetrical haemorrhage ..
 PCV transfusion , if available is preferred than
Whole Blood .

28. FOLATE DEFICIENCY ANAEMIA ---

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. FOLATE DEFICIENCY ANAEMIA ---
 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.

32. FOLATE DEFICIENCY ANAEMIA ---
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

33. NURAL TUBE DEFFECT: 

34. 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

35. 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 .

36. TREATMENT
 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.

37. COBALAMINE (VIT .B12 ) DEFICIENCY
 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.

38. COBALAMINE (VIT .B12 ) DEFICIENCY
 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 .

40. 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 .

41. 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.

42. THALASSAEMIA
 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. 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

44. 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 is has normal Hb Or Trait only
Pregnancy can be continued and mange the
anaemia by blood transfusion as per need.

45. 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 .

46. 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

47. 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.

48. 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.

49. 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.

50. 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