IRON DEFICIENCY ANAEMIA

 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
ETIOLOGY OF IRON DEFICIENCY ANAEMIA
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
 EFFECTS OF ANAEMA IN PREGNANCY
 . 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 c. section
 Fetus: . IUGR
. Preterm birth
. LBW
. Depleted Fe store
. Delayed Cognitive function.
 INVESTIGATIONS

 Hb
 Haematocrit
 RBC Indices:
- Low MCV
- Low MCH
- Low MCHC
- Low PCV
 Peripheral blood picture :
Microcytic Hypochromic anaemia .
 INVESTIGATIONS
 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.
 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 expecred in 7-14 d
Blood transfusion:
 may be required to treat severe anaemia near term or when
some other complication such as placenta praevia present.
 Gross anaemia
 Packed red cells transfusion (Under cover of loop

diuretic)
 Exchange transfusion (Under cover of loop diuretic)
 MANAGEMENT
Side effect of Fe Oral therapy:
. G. I upset.
. Constipation.
. Diarrhoea.
Parentral:
- skin discolouration
- local abscess
- allergic reaction
- Fe over load.
 MEGALOBLASTIC ANAEMIA
 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
FOLATE DEFICIENCY ANAEMIA
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.
 FOLATE DEFICIENCY ANAEMIA

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.
 FOLATE DEFICIENCY ANAEMIA
Diagnosis: Increased MCV ( > 100 fl)
Peripheral smear: - Macrocytosis, hypochromia
- Hypersegmented neutrophils
(> 5 lobes)
- Neutropenia
- Thrombocytopenia

Low Serum folate level.

Low RBC folate.
 FOLATE DEFICIENCY ANAEMIA
 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.
 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.
 HAEMOGLOBINOPATHIES.
 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.
 HAEMOGLOBINOPATHIES
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)
 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.
 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.
 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.
 Sickle Cell Disease (SCD)

 Sickeling crises frequently occurs in pregnancy,

puerperium &in state of hypoxia like G/A and Hag.
 Increased incidance 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