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