This document summarizes different types of anemia seen in pregnancy. It discusses physiological anemia of pregnancy and pathological anemias including deficiency, hemorrhagic, hereditary, and those caused by bone marrow insufficiency or infection. Specific hereditary anemias covered are thalassemias, sickle cell disease, and other hemoglobinopathies. Causes, symptoms, investigations, and management are described for different types of anemia.

1. Classification of anemia
• Physiological anemia of pregnancy
• Pathological
– Deficiency anemia
• Fe deficiency
• Folic acid deficiency
• Vit B12
• Protein deficeincy
– Haemorrhagic
• Acute – following bleeding in early months or APH
• Chronic – Hookworm infestation, bleeding piles

2. – Hereditary
• Thalassemias
• Sickle cell haemoglobinopathies
• Other haemoglobinopathies
• Hereditary haemolytic anemias
– Bone marrow insufficiency
– Anemia of infection
– Chronic disease (renal) or neoplasm

3. Physiological anemia
• In pregnancy:
– Increase in plasma volume, RBC volume and Hb
mass
– Marked demand of extra iron specially in the second
half which cannot be overcome by diet.
• Thus, there always remains a physiological iron
deficiency state during prenancy.
• As a result, there is not only a fall in Hb conc and
hematocrit value in the second half of pregnancy,
but there is also assoc low serum iron.

4. Criteria for physiological anemia
• Hb – 10gm%
• RBC: 3.2 million/mm3
• PCV: 30%
• Peripheral smear: normal morphology of RBC
with central pallor

5. Why anemia during pregnancy???
• The woman who has got sufficient iron reserve
and is on balanced diet – unlikely
• But if iron reserve is inadequate or absent :
– Increased demands of iron
– Diminished intake of iron
– Disturbed metabolism
– Pre – pregnant health status
– Excess demand: multiple pregnancy, rapidly
recurring pregnancy.

7. SYMPTOMS

10. O/E

11. • Soft murmur
• Oedema
• Crepitations – base of lungs

12. Investigations
• If Hb < 9 gm%  should be sent for
investigations
• Objectives:
– Degree of anemia
– Type of anemia
– Cause of anemia

13. Degree of anemia
• Hb
• Total Red cell count
• Determination of PCV
Mild Between 8 -7 gm%
Moderate Less than 8 – 7gm%
Severe Less than 7gm%

14. Type of anemia
• Peripheral blood smear
• Haematological indices: MCHC, MCV and MCH
• Serum iron value

15. Cause of anemia
• Examination of stool
• Urine examination

16. Complication of severe anemia
• During pregnancy:
– Pre-eclampsia
– Intercurrent infection
– Heart failure
– Preterm labour
• During labour:
– Uterine inertia
– PPH
– Cardiac failure
– shock

17. • Puerperium:
– Puerperal sepsis
– Subinvolution
– Failing lactation
– Pulmonary embolism

18. Risk period
• At about 30 – 32 weeks of pregnancy
• During labour
• Immediate following delivery
• Any time in puerperium specially 7 – 10 days
following delivery

19. Effects on baby:
• LBW : increased incidence
• Intra uterine death

20. Prognosis:
• Maternal: if detected early  good
• Fetal: if detected early and responsive to
treatment , the fetal prognosis is not too bad.
– But in severe and neglected cases, there can be
prematurity

21. Treatment
• Prphylactic:
– Avoidance of frequent child births
– Supplementary iron therapy
– Dietary prescription
– Adequate treatment
– Early detection of falling Hb level is to be made

22. • Curative:
– Hospitalisation
– General treatment:
• Diet
• To improve appetite and facilitate digestion
• To eradicate even minimal septic focus
• Effective therapy to cure the disease

23. Specific therpay:
• Depends on:
– Severity
– Duration of pregnancy
– Assoc complicating factors

24. Iron therapy
• Oral route:
– Drawbacks:
• Intolerance
• Unpredictable absorption rate
– Response:
• Sense of well being
• Increased appetite
• Improved outlook of the patient
• Haematological examination
• Rise in Hb level
– Rate of improvement – within 3 weeks

25. – Failure:
• Improper typing of anemia
• Defective absorption
• Pt fails to take iron
• Concurrent blood loss
– Contraindication:
• Intolerance
• Severe anemia in advanced pregnancy

26. • Parenteral therapy:
– Intravenous and Intramuscular
– Indications:
• Contraindications of oral therapy
• Pt not co-operative to take oral iron
• Cases seen for the first time during the last 8 – 10
weeks in severe anemia

27. • Intravenous route:
– Total dose diffusion: deficit of iron is calculated and
the total amount of iron required is administered by a
single sitting intravenous infusion
– Advantages:
• Eliminates repeated and painful intramuscular
injections
• Treatment completed in a day
• Less costly

28. • Intramuscular therapy:
– Total dose to be administered is calculated
– After an initial dose of 1ml, the injections are given
daily or on alternate days in doses of 2ml
intramuscularly.
– Drawbacks:
• Painful
• Chance of abscess
• Reactions

29. • Blood transfusion:
– Limited. But indications are:
• PPH
• Severe anaemia in later months of pregnancy
• Refractory anemia
• Assoc infection.
– Quality and quantity: fresh. Only packed cell. 80 –
100 ml at a time
– Advantages:
• Increased oxygen carrying capacity of the blood
• Hb may be utilised for the formation of new red
cells.
• Stimulated erythropoiesis
• Improvement expected after 3 days

31. • There is derangement in red cell maturation with
the production in the bone marrow of abnormal
precursors known as megaloblasts due to
impaired DNA synthesis.

32. • Vit B12 or folate defieciency or both.
• Vit B12 deficiency is rare in pregnancy.
• In pregnancy, due to folic acid deficiency.

33. Causes
• Megaloblastic anaemia of pregnancy (temperate
climate)
• Nutritional megaloblastic anaemia
• Addisonian pernicious anaemia (rare)
• Megaloblastic anaemia of malabsorption
syndrome.

34. Folic acid deficiency…
• Inadequate intake due to:
– Nausea, vomiting, loss of appetite.
– Dietary insufficiency – green leafy veg, cauliflower,
spinach, liver, kidney
• Increased demand:
– Increased maternal tissue including red cell volume.
– Developing product of conception.
• Diminished absorption:
• Abnormal demand:
– Twins, infection, haemorrhagic states.
• Failure of utilisation:
– Anticonvulsant drugs.

35. • Diminshed storage:
– Hepatic disorders and vitamin c deficiency.
• Iron deficiency anaemia:

36. Incidence
• 0.5 – 3%
• Common in multiparae and multiple pregnancy.

37. Clinical features

38. O/E

39. Haematological examination and other
blood values
• Hb – 10gm%
• Stained blood film: hypersegmentation of the
neutrophils, macrocytosis and anisocytosis.
Megaloblasts.
• MCV- 100 µm3
• MCH –high, MCHC –normal
• Associated leucopenia and thrombocytopenia
• Serum iron is normal or high
• Serum folate – 3ng/ml
• Serum B12 level below <90 pg/ml
• Bone marrow – megaloblastic erythropoiesis

40. COMPLICATIONS
• Abortion
• Dysmaturity
• Prematurity
• Abruptio placentae
• Fetal malformation

41. Prophylactic therapy
• All woman of reproductive age should be given
400µg of folic acid daily.
• Additional amount (4mg) should be given where
demand is high.

42. HAEMOGLOBINOPATHIES

43. SICKLE CELL ANAEMIA

44. • Hereditary disorders in which the red cells contain
Hb-S.
• Produced by substitution of valine for glutamic
acid at the position 6 of the β-chain of normal
haemoglobin.

45. Pathophysiology
• Red cells with HbS in oxygenated state behave
normally but in the deoxygenated state it
aggregates, polymerises and distort the red cells
to sickle.
• These sickle shaped cells block the
microcirculation due to their rigid structure.

46. Effects on pregnancy
• Increased incidence of abortion,prematurity,
IUGR and fetal loss.
• Perinatal mortality is high.
• Preclampsia, postpartum haemorrahage and
infection is increased.

47. Effects on the disease.
• There is chance of sickle cell crisis which usually
occurs in the last trimester.
• Haemolytic crisis
• Painful crisis.

48. Management
• Preconceptional counselling
• During pregnancy: antenatal supervision, regular
blood transfusion at 6 weeks interval.
• Contraception: sterilisation, oral pill, barrier
method is ideal.

49. Thalassaemia syndromes
• Commonly found genetic disorders of the blood.
• Basic defect is a reduced rate of globin chain
synthesis.
• As a result, the red cellsbeing formed with an
inadequate haemoglobin content.
• Types – alpha and beta (depending upon the
chain)

50. Alpha thalassaemia
• Incompatible with life.
• Α-peptide chain production is controlled by 4
genes, located on chromosome 16. Depending
upon the degree of deficient synthesis – 4 clinical
types.
• Mutation of one gene: no clinical or laboratory
abnormalities. Silent carrier

51. • Mutation in 2 – 4 genes: minor. Often goes
unrecognised and pregnancy is well tolerated.
• Mutation in 3 – 4 genes: Hb H disease. 
hemolytic anaemia.
• Mutation in all four genes: major. No alpha globin
chain. Fetus dies either in utero or soon after
birth.

52. Beta thalassemia
• beta chain production is directed by 2 genes –
one on each copy of chromosome 11.
• Major – when mutation affect both the genes. –
red cell destruction- no erythropoiesis – blood
transfusion necessary for survival.
• Minor – mutation of one gene. – can tolerate
pregnancy –oral folic acid supplementation is
continued.