Dr.Suresh Babu Chaduvula
Dept. of OBGYN
College of Medicine
King Khalid University
Commonest medical disorder.
High incidence in underdeveloped countries
Increased Maternal morbidity & mortality
Increased perinatal mortality
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
There are 3 main causes:
1- Erythrocyte production: (hypo proliferative
. Fe deficiency
. Folic acid
2- RBC destruction:
3- RBC loss:
90% anemia in pregnancy is due to Fe deficiency
• Plasama volume 50% (by 34weeks)
• But RBC mass only 25%
• Results in haemodilution :
No change in MCV or MCH
2-3 fold increase in Fe requierment.
10-20 fold increase in folate requirement
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
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.
Symptoms usually in severe anaemia
. Mother :
High output Cardiac failure (more likely if precelampsia present.
inadequate tissue oxygenation increase requirments for excessive
blood flow )
Predisposes to infection
Risk of thrombo-embolism
Delayed general physical recovery esp. after cesarean section
. Preterm birth
. Depleted Fe store
. Delayed Cognitive function.
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
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.
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.
Urine for haemturia.
Stool examination for ova ,cyst and occult blood.
Ankylostoma duodenale – a hook worm that will
suck blood from small intestine.
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 anemia
Presence of additional risk factor
Recommended supplementation for non-anaemiac 30 -
60mg /day of elemental iron
Anemic gravidas 120 –240mg / per day
Intolerance to iron tablets – enteric coated tablet /
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
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)
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-
Marked increase in reticulocyte count expected in 7-14 d
may be required to treat severe anemia near term or
when some other complication such as placenta previa
Packed red cells transfusion (under cover of loop
Exchange transfusion (under cover of loop diuretic)
Side effect of Fe Oral therapy:
. G. I upset.
- skin discolouration
- local abscess
- allergic reaction
- Fe over load.
Complicates upto 1% of pregnancies
Characterized by :
- RBC with high MCV
- White blood cells with altered morphology
Usually caused by :
- Folate deficiency may occur after
exposure to sulfa drugs or hydroxyurea
- Vitamin B12 deficiency
At cellular level
Folic acid reduced to Dihydrofolicacid then to
Tetrahydro-folicacid (THF) is required for cell growth &
So more active tissue reproduction & growth - more
dependent on supply of folic acid.
So bone marrow and epithelial lining are therefore at
Folic acid deficiency more likely if
. Woman taking anticonvulsants.
. Multiple pregnancy.
. Hemolytic anemia; thalasemia H.spherocytosis
Pre-conception deficiency cause neural
tube defect and cleft palate etc.
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.
- 0.5-1.0mg folic acid/day
If Family history of neural tube defect
- 4mg folic acid/day.
It is rare
Occurs in patients with gastrectomy , ileitis, illeal
resection, pernicious anaemia, intestinal parasites.
Vitamin B12 level < 80 pico g/ml
Treatment of B12 Deficiency:
Vit B12 1mg I/M weekly for 6 weeks.
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.
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)
The synthesis of globin chain is partially or completely
suppressed resulting in reduced Hb. content in red
cells with shortened life span.
- Alpha thalassemia.
- Beta thalassemia:
Beta Thallassemia trait
Heterozygous inheritance from one parent.
Most frequent encountered variety.
Partial suppression of the Hb. synthesis.
Investigations: Hb----around 10 g/dl.
Red cell indices: low MCV.
Diagnostic test: Hb. Electrophoresis.
Same as normal woman in pregnancy.
Frequent Hb. Testing.
Iron & folate supplements in usual dose.
Parenteral iron should be avoided. because of iron
If not responded ---I/M folic acid.
blood transfusion close to time of delivery.
Homozygous inheritance from both parents.
Diagnosed in paediatric era.
T/m: is blood transfusion.
Both heterozygous & homozygous forms
Alpha thallassaemia trait.
Alpha thallassaemia major
Autosomally inherited .
HbS - susceptible to hypoxia, when oxygen supply
Hb precipitates & makes the RBCs rigid & sickle
Compound heterozygous---HbSC etc.
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
- Hb. Electrophoresis
- Sickling test is screening test
- No curative Tx.
- only symptomatic
- Well hydration, effective analgesia, prophylactic
antibiotics, O2 inhalation, folic acid, oral iron
supplement (I/V iron is contraindicated), blood
Low threshold of assisted delivery
Continue iron &folate therapy for 3 months after
Appropriate contraceptive advice