jgjfn hhff jfd

1. ANAEMIA IN PREGNANCY
BY
Dr. Shumaila Zia

2. ANAEMIA IN PREGNANCY
 Commonest medical disorder.
 High incidence in underdeveloped countries
 Increased Maternal morbidity & mortality
 Increased perinatal mortality

3. ANAEMIA IN PREGNANCY
Definition: By WHO
Hb. < 11 gm /dl
(or haematocrit <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. ETIOLOGY
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. Physiological changes in
pregnancy
• 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 Anaemias in pregnancy
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 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

9. 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

10. 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.

11. INVESTIGATIONS
 Hb
 Haematocrit
 RBC Indices:
- Low MCV
- Low MCH
- Low MCHC
- Low PCV
 Peripheral blood picture :
Microcytic Hypochromic anaemia .

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.

14. 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

15. MANAGEMENT
 Recommended supplementation for non-anaemiac
30 - 60mg /day of elemental iron
 Anaemic gravidas 120 –240mg / per day
 In tolerance 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

16. 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 neede =
(Normal Hb – Pt. Hb)* Wt in Kg*2.21+1000)

17. 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)

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

19. 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

20. 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.

21. 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.

22. 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.

23. 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.

24. 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.

25. 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.

26. 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)

27. 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

28. 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.

29. 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.

30. 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.

31. 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.

32. 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

33. SCD
 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

35. 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