This document summarizes iron deficiency anemia in pregnancy. It discusses that anemia is the most common medical disorder globally, with high rates in underdeveloped countries. Anemia increases maternal and perinatal mortality. The document defines the classifications of anemia severity based on hemoglobin levels. The main causes of anemia in pregnancy are listed as iron deficiency, folic acid deficiency, and vitamin B12 deficiency. Risk factors, clinical features, investigations, and management approaches are all outlined in detail.

1. Dr.Suresh Babu Chaduvula
Professor
Dept. of OBGYN
College of Medicine
King Khalid University
Abha, KSA

2.  Commonest medical disorder.
 High incidence in underdeveloped countries
Importance:
 Increased Maternal morbidity & mortality
 Increased perinatal mortality

3. Definition: By WHO
Hb. < 11 gm /dl
(or Hematocrit <32%).
Mild anaemia -------- 9 -10.9 gm /dl
Moderate anaemia--- 7-8.9 gm /dl
Sever anaemia-------- < 7gm /dl
Very sever anaemia-- < 4gm/dl

4. There are 3 main causes:
1- Erythrocyte production: (hypo proliferative
anemia )
. Fe deficiency
. Folic acid
Vitamin B12
2- RBC destruction:
3- RBC loss:
90% anemia in pregnancy is due to Fe deficiency

5. • Plasama volume 50% (by 34weeks)
• But RBC mass only 25%
• Results in haemodilution :
• Hb
Haematocrit
RBC count
 No change in MCV or MCH
 2-3 fold increase in Fe requierment.
 10-20 fold increase in folate requirement

7. Common types:
 Nutritional deficiency anaemias
- Iron deficiency
- Folate deficiency
- Vit. B12 deficiency
 Haemoglobinopathies:
- Thallassemias
- SCD
Rare types:
- Aplastic
- Autoimmune hemolytic
- Leukemia
- Hodgkin’s disease
- Paroxysmal nocturnal haemoglobinurea

8.  Iron required for fetus and placenta ------- 500mg.
 Iron required for red cell increment ------- 500mg
 Post partum loss --------- 180mg.
 Lactation for 6 months - 180mg.
 Total requirement -------1360mg
 350mg subtracted (saved as a result of amennorrhoea)
 So actual extra demand ----------------------1000mg
 Full iron stores --------------------------------1000mg

9. Depleted iron stores – dietary lack, chronic renal
failure, worm infestation, chronic menorrhagia
Chronic infections: ( like malaria)
Repeated pregnancies :
- with interval < 1 year
- blood loss at time of delivery
- multiple pregnancy.
CLINICAL FEATURES
Symptoms usually in severe anaemia
- Fatigue
- Giddiness
- Breathlessness

10.  . Mother :
 High output Cardiac failure (more likely if precelampsia present.
inadequate tissue oxygenation increase requirments for excessive
blood flow )
 PPH
 Predisposes to infection
 Risk of thrombo-embolism
 Delayed general physical recovery esp. after cesarean section
 Fetus: .IUGR
. Preterm birth
. LBW
. Depleted Fe store
. Delayed Cognitive function.

11.  Hb
 Haematocrit or PCV
 RBC Indices:
- Low MCV
- Low MCH
- Low MCHC
 Peripheral blood picture :
Microcytic Hypochromic
anemia .

12.  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.
INVESTIGATIONS

13.  Serum transferrin receptor(TfR) : present on all
cells as transmembrane protien that binds
transferrin iron and transfer it to cell interior.
Increased in iron def. anemia.
 Bone marrow examination.
 RFTS/LFTS.
 Urine for haemturia.
 Stool examination for ova ,cyst and occult blood.
 Ankylostoma duodenale – a hook worm that will
suck blood from small intestine.

14.  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

15.  Choice of method:
It depends on three main factors:
 Severity of the anemia
 Gestational Age.
 Presence of additional risk factor

16.  Recommended supplementation for non-anaemiac 30 -
60mg /day of elemental iron
 Anemic gravidas 120 –240mg / per day
 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

17.  Moderate anaemia: 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 needs =
(Normal Hb – Pt. Hb) X Wt in Kg X 2.21+1000)

18. 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)

19. Side effect of Fe Oral therapy:
. G. I upset.
. Constipation.
. Diarrhoea.
Parentral:
- skin discolouration
- local abscess
- allergic reaction
- Fe over load.

20.  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

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

22. 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.

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

24.  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 Family history of neural tube defect
- 4mg folic acid/day.

25.  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.

26.  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.

27. 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)

28.  The synthesis of globin chain is partially or completely
suppressed resulting in reduced Hb. content in red
cells with shortened life span.
 TYPES:
- Alpha thalassemia.
- Beta thalassemia:
. Major
. minor

29.  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.

30.  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.

31.  Homozygous inheritance from both parents.
 Sever anaemia.
 Diagnosed in paediatric era.
 T/m: is blood transfusion.
.

32. ALPHA THALASSAEMIA:
 Both heterozygous & homozygous forms
exist.
 Alpha thallassaemia trait.
 HbH disease.
 Alpha thallassaemia major

33.  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.

34.  Sickeling crises frequently occurs in pregnancy,
puerperium and in state of hypoxia.
 Increased incidence of abortion and still birth
growth restriction, premature birth and intrapartum
fetal distress with increased perinatal mortality.
 Sickle cell trait:(carrier state)
Does not pose any significance clinical problems

35.  Diagnosis:
- Hb. Electrophoresis
- Sickling 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 contraindicated), blood
transfusion

37.  Comfortable Position
 Adequate analgesia
 O2 inhalation
 Low threshold of assisted delivery
Prophylactic Ergometrine
 Prophylactic antibiotics
 Continue iron &folate therapy for 3 months after
delivery
 Appropriate contraceptive advice

38. Thank You All