1. The document discusses various types of anemia that can occur during pregnancy including physiological anemia, iron deficiency anemia, megaloblastic anemia, and hemoglobinopathies like sickle cell anemia and thalassemia. 2. It provides details on the causes, signs and symptoms, complications, investigations, and management of these anemias. 3. Specific attention is given to megaloblastic anemia caused by folic acid deficiency which is a common form of anemia during pregnancy, as well as the effects and management of sickle cell anemia and thalassemia during pregnancy.

1. ANAEMIA IN PREGNANCY
DR SALINI MANDAL B.G.
ASST PROFESSOR
DEPT OF OBG
FMHMC

2. 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

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

4. 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.

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

6. 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.

8. SYMPTOMS

11. O/E

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

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

14. 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%

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

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

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

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

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

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

21. 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

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

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

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

25. 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

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

27. • 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

28. • 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

29. • 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

30. • 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

32. • 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.

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

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

35. 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.

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

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

38. Clinical features

39. O/E

40. 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

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

42. 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.

43. HAEMOGLOBINOPATHIES

44. SICKLE CELL ANAEMIA

45. • 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.

46. 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.

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

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

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

50. 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)

51. 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

52. • 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.

53. 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.