Anemia is a common medical disorder in pregnancy that increases risks for both mother and baby. The document defines anemia in pregnancy according to WHO standards and describes the main causes as decreased red blood cell production or increased destruction, with 90% of cases due to iron deficiency. Evaluation involves hematological indices and iron studies. Management focuses on iron supplementation orally or parenterally depending on severity, with blood transfusions for severe cases. Specific attention is given to nutritional deficiencies like iron, folate, vitamin B12 and hemoglobinopathies.

1. Anemia in Pregnancy
By Dr. Ashok Moses
Medical Advisor Franco-Indian
Pharmaceuticals Ltd.

2. Anemia in Pregnancy
• Commonest medical disorder.
• High incidence in underdeveloped countries.
• Increases maternal morbidity and mortality.
• Increases peri natal mortality.

3. Anemia in Pregnancy
Definition by WHO.
• Hemoglobin less than 11.0 gms/dl or hematocrit
<32.
Classification
• Mild anemia – 9.0 – 10.9 gms/dl.
• Moderate -----7.8 – 9.0 gms/dl.
• Severe ------ < 7.0 gms/dl
• Very severe ----- < 4.0 gms/dl

4. ETIOLOGY
• There are 3 main causes :
1. Decreased erythrocyte production
(Hypoproliferative anemia)
• Iron defficiency
• B 12 defficiency
• Folate defficiency
2. RBC destruction
3. RBC Loss
*90 % of anemia in pregnancy is due to iron
defficiency

5. Physiological changes in pregnancy
• Plasma volume increases 50% by 34 weeks.
• RBC mass increases by only 25%.
• Results in hemodilution. i.e reduced Hb,
hematocrit, RBC count.
• No change in MCV or MCH.
• 2-3 fold increase in Fe requirement.
• 10-20 fold increase in folate requirement.

6. Normal iron metabolism
- The primary function is oxygen transport.
- Iron is absorbed by duodenum and jejunim
- Average total body iron content 3500-4000 mg.
- Approximately 2/3 found in hemoglobin,
- Iron is also stored in RE cells (BM, Spleen and liver) as
hemosiderin and ferratin.
- Also iron found in myglobin and myeloperoxidase and
in certain electron transfer.
- Iron is more stable in ferric state (Fe+++) than in ferrous
state (Fe++).

8. Iron + Hem
Iron Metabolism

9. Absorption of Iron
http://youtu.be/umtxr9SQoI8

10. • Dietary iron:
• Iron is present in food as ferric hydroxides (ferric-
protein complexes and hem-protein complexes).
• -meat, liver
• -vegetables, eggs.
• -The average diet contains 10-15mg and only 5-10% is
normally absorbed.
• Iron requirements:
• It varies depending on sex and age:
• Male/female 0.5-1 mg/day
• Pregnant female 1-2 mg/day
• Children 0.5 mg/day

11. Common anemia's in pregnancy
• Common
• Nutritional Iron, B12, and Folate defficiency.
• Hemoglobinopathies Thallasemias, Sickle cell
anemias.
• Rare causes: Aplastic anemia, Auto immune
hemolytic, Leukemia, Hodgkins disease, PNH.

12. Clinical features:
When ID is developing, the RE stores
(hemosiderin and ferritin) become completely
depleted before anemia occurs.
At an early stage, no clinical abnormalities.
Later, patient may develops general symptoms
and signs of anemia.
In severe case of IDA ridged or spoon nails

13. Effects of anemia in pregnancy
• Mother
1. High output cardiac failure.( More likely if
pre-ecclamsia present)
2. PPH.
3. Predisposition to infection.
4. Risk of thrombo embolism.
5. Delayed general recovery especially after CS.

14. Effects on fetus
1. IUGR
2. Preterm birth
3. LBW
4. Depleted Fe store
5. Delayed cognitive function

15. Laboratory findings
Red cell indices:
Low Hb conc.
MCV, MCH, MCHC*
Blood film:
Hypochromic microcytic Picture.
Occasional Target cells.
Pencil shaped poikilocytes.
Normal reticulocyte count.
Bone marrow iron:
Normal to hypercellular.
RBC precursors are increased in number.
Iron stain negative.
Chemical testing on serum:
Serum iron Decreased
Transferrin/TIBC Normal to High
Serum ferritin Decreased (Very low)

16. Hypochromic Microcytic picture (IDA)
--ve BM Iron Stain +ve

17. • Serum iron decreased (<12 micro mol / l)
• Total iron binding capacity :TIBC in non-
pregnant state is 33% saturated with iron
.when serum iron level fall ,<15% ofTIBC
saturated.by fall in saturation,the TIBC
INCREASED.
• S. ferritin :In healthy adults ferritin circulate in
plasma in range of 15_300 pg/l. in iron
deficiency anemia it is the first test to become
abnormal

18. MANAGEMENT
• Objectives:
1- To achieve a normal Hb by end of pregnancy
2- To replenish iron stores
• Two ways to correct anaemia:
I- Iron supplementation . Oral Fe
. Parenteral Fe
II- Blood transfurion
• Choice of method:
It depends on three main factors:
• Severity of the anaemia
• Gestational Age.
• Presence of additional risk factor

19. MANAGEMENT
• Recommended supplementation for non-anemic
30 - 60mg /day of elemental iron
• Anemic gravida’s 120 –240mg / per day
• If intolerance to iron tablets – enteric coated
tablet / liquid suspension
• Supplementation with folic acid + Vit C.
• Therapeutic results after 3 weeks – rise in Hb %
level of 0.8gm/dl/ week with good compliance.
• Treatment continued in the postpartum period
to fill the stores

20. Elemental iron
• What is elemental iron?
Iron supplements have two different
amounts of iron listed on the same package.
The higher number is the total amount of iron
in the supplement. The second, smaller
number is the amount of elemental iron.

21. Elemental iron
• Elemental iron is the total amount of iron in the
supplement available for absorption by the body. Each
type of iron has a different percent of elemental iron.
For instance:
• Carbonyl has 100% elemental iron.
• Ferrous fumarate has approximately 33% elemental
iron.
• Ferrous sulfate has 20% elemental iron.
• Ferrous gluconate has 12% elemental iron.
• Ferric ammonium citrate has 18.5 % elemental iron (
Dexorange).

22. Elemental iron
• But the ferrous salts have a lower tolerability
when compared with the ferric salts due to the
high incidence of side effects on the GI Tract with
ferrous salts.
• The amount of elemental iron in a supplement is
typically listed in the Supplement Facts panel. In
addition, some iron supplements will indicate the
total milligrams of elemental iron on the front of
the package making it easy for patients to
compare different iron supplements.

23. Elemental iron
• Ferric Ammonium Citrate (Dexorange) is one
of the best iron supplements. Ferric
Ammonium Citrate provides an optimum
tolerance of the iron preparation, which is of
utmost importance in maintaining long term
patient compliance to any hematinic therapy.

24. MANAGEMENT
• Severe anaemia: (Hb < 8gm/dl)- preferably
parenteral theraphy in the form of I/M or I/V
iron
- I/M : ( Iron sorbitol) with “Z” technique
- I/V : (iron sucrose)
• Iron needed = (Normal Hb – Pt. Hb) x Wt in kg x
2.21+1000)

25. MANAGEMENT
Dose given I/M or I/V by slow push 100mg / day or the entire
dose given in 500 ml N/S slow I/V infusion over 1-6 hours
• Marked increase in reticulocyte count expected in 7-14 d
Blood transfusion:
• may be required to treat severe anemia near term or when
some other complication such as placenta previa present.
• Gross anemia
• Packed red cells transfusion (Under cover of loop
diuretic)
• Exchange transfusion (Under cover of loop diuretic)

26. MANAGEMENT
Side effect of Fe Oral therapy:
. G. I upset.
. Constipation.
. Diarrhoea. (More with ferrous salts).
Parentral:
- skin discolouration
- local abscess
- allergic reaction
- Fe over load.

27. MEGALOBLASTIC ANEMIA
• Complicates upto 1% of pregnancies
• Characterized by :
- RBC with high MCV
- White blood cells with altered morphology
(hypersegmented neutrophils).
• Usually caused by :
- Folate deficiency may occur after exposure
to sulfa drugs or hydroxyurea
- Vitamin B12 deficiency

28. FOLATE DEFICIENCY ANEMIA
At cellular level
Folic acid reduced to Dihydrofolicacid then
Tetrahydro-folicacid . (THF) e is required for cell
growth & division.
So more active tissue reproduction & growth more
dependant on supply of folic acid.
So bone marrow and epithelial lining are therefore
at particular risk.

29. FOLATE DEFICIENCY ANEMIA
Folic acid deficiency more likely if
. Woman taking anticonvulsants.
. Multiple pregnancy.
. Hemolytic anemia; thalasemia
H.spherocytosis
Maternal risk:
Megaloblastic anemia
Fetal risk:
Pre-conception deficiency cause neural
tube defect and cleft palate
etc.

30. FOLATE DEFICIENCY ANEMIA
• Diagnosis: Increased MCV ( > 100 fl)
• Peripheral smear: - Macrocytosis, hypochromia
• - Hypersegmented neutrophils
• (> 5 lobes)
• - Neutropenia
• - Thrombocytopenia
• Low Serum folate level.
• Low RBC folate.

31. FOLATE DEFICIENCY ANEMIA
Daily folate requirement for :
Non pregnant women -- 50 -100 microgram
Pregnant woman –-------- 300-400 microgram
Usually folic acid present in diets like fresh fruits
and vegetables and destroyed by cooking.
Folate deficiency:
- 0.5-1.0mg folic acid/day
If F/Hx. of neural tube defect
- 4mg folic acid/day

32. Vitamins B12 Deficiency
It is rare
Occurs in patients with gastrectomy , ileitis, illeal
resection, pernicious anaemia, intestinal
parasites.
Diagnosis:
Peripheral smear
Vitamin B12 level < 80 pico g/ml
Treatment of B12 Deficiency:
Vit B12 1mg I/M weekly for 6 weeks.

33. HEMOGLOBINOPATHIES
• Normal adult Hb. after age of 6 month,
• HbA---97%, HbA2---(1.5-3.5%), HbF2--<1%.
• 4 Globin chains associated with haem complex.
• Hb. A = 2 alpha +2 beta globin chains.
• Hb.A2= 2alpha+2 delta globin chains.
• Hb.F = 2 alpha+ 2 gamma globin chains.
• Hb. synthesis is controlled by genes.
• Alpha chains by 4 gene,2 from each parent.
• Beta chains by 2 genes ,1 from each parent.

34. HEMOGLOBINOPATHIES
DEFINITION:
• Inherited disorders of haemoglobin.
• Defect may be in:
- Globin chain synthesis------thallassemia.
- Structure of globin chains-sickle cell disease.
• Hb.abnormalities may be:
- Homozygous = inherited from both parents.
(Sufferer of disease)
- Hetrozygous = inherited from one parent.
(Carrier/trait of disease

35. THALASSAEMIAS
• The synthesis of globin chain is partially or
completely suppressed resulting in reduced Hb.
content in red cells,which then have shortened
life span.
• TYPES:
- Alpha thalassaemia.
- Beta thalassaemia:
. Major
. Minor

36. Beta thallassemia minor
• Beta Thallassemia trait
• Heterozygous inheritance from one parent.
• Most frequent encountered variety.
• Partial suppression of the Hb. synthesis.
• Mild anaemia.
Investigations: Hb----around 10 g/dl.
• Red cell indices: low MCV.
low MCH.
normal MCHC.
• Diagnostic test: Hb. Electrophoresis

37. Beta Thallassemia Minor
• Management:
• Same as normal woman in pregnancy.
• Frequent Hb. Testing.
• Iron & folate supplements in usual dose.
• Parenteral iron should be avoided. because
of iron overload.
• If not responded ---I/M folic acid.
• blood transfusion close to time of delivery.

38. Beta Thallassaemia Major
• Homozygous inheritance from both parents.
• Sever anaemia.
• Diagnosed in paediatric era.
• T/m: is blood transfusion.
ALPHA THALASSAEMIA:
• Both heterozygous & homozygous forms exist.
• Alpha thallassaemia trait.
• HbH disease.
• Alpha thallassaemia major.

39. SICKLE CELL SYNDROME
• Autosomally inherited .
• Structural abnormality.
• HbS - susceptible to hypoxia, when oxygen
supply is reduced.
• Hb precipitates & makes the RBCs rigid & sickle
shaped.
• Heterozygous----HbAS.
• Homozygous-----HbSS.
• Compound heterozygous---HbSC etc.

40. SICKLE CELL SYNDROME
• Sickling crises frequently occurs in pregnancy,
puerperium &in state of hypoxia .
• Increased incidence of abortion and still birth
growth restriction, premature birth and intra
partum fetal distress with increased perinatal
mortality.
• Sickle cell trait:(carrier state)
Does not pose any significance clinically.

41. SICKLE CELL SYNDROME
• Diagnosis:
- Hb. Electrophoresis
- Sickledext test is screening test
• Management:
- No curative Tx.
- only symptomatic
- Well hydration, effective analgesia, prophylactic
antibiotics, O2 inhalation, folic acid, oral iron
supplement (I/V iron is C/I), blood transfusion

43. Management During labour
• Comfortable Position
• Adequate analgesia
• O2 inhalation
• Low threshold of assisted delivery
• Avoid ergometrine
• Prophylactic antibiotics
• Continue iron &folate therapy for 3 mo after
delivery
• Appropriate contraceptive advice