ANAEMIA IN PREGNANCY

Y Commonest medical disorder in pregnancy

Y Out of estimated 160 million deliveries occurring annually
in the world, approx 6,00,000 women die from the
complications of pregnancy & child birth (W.H.O 1996).
Y Anaemia is responsible for 40-
40-60% of maternal deaths in
developing countries. It also increases perinatal mortality
and morbidity rates (W.H.O 1997).
 |EFINITION

Y Anaemia is a condition of low circulating haemoglobin in

which haemoglobin concentration has fallen below the
threshold lying at two standard deviations below the
median value for a healthy matched population.
Y W.H.O defines anaemia in pregnancy as haemoglobin
concentration of less than 11 g/dl and haematocrit of less
than 0.33.
Y The cut-
cut-off point suggested by the United States Centers
for disease control is 10.5 gm/dl in the second trimester.
 ERYTHROPOIESIS

Y Confined to the bone marrow in adults

Y RBCs are formed through stages of pro-
pro-normoblast ²
normoblast ² reticulocytes ² mature non-
non-nucleated
arithrocyte.
Y After a life span of 120 days RBCs degenerate and
haemoglobin is broken down into haemosiderin and bi-
bi-
pigment.
 ERYTHROPOIESIS (Contd.)

Y For proper erythropoiesis adequate nutrients are needed:

1. Minerals: Iron, traces of copper, cobalt and zinc.
2. Vitamins: Folic Acid, Vitamin B12, Vitamin C,
Pyridoxine and riboflavin
3. Proteins: For synthesis of globin moiety.
4. Hormones: Androgens and thyroxine.
 ERYTHROPOIETIN

Erythropoietin is a hormone produced by kidneys (90%) and

the liver (10%)
Y Increased secretion occurs during pregnancy due to
placental lactogen and progestrone.
Y Eryhtropoietin increases red cell volume by stimulating
stem cells in the bone marrow.
Y In addition to common deficiency of folic acid and iron,
there is a growing body of evidence to implicate vitamin
A in nutritional anaemia.
PREVALENCE OF ANAEMIA
ACCOR|ING TO AGE

   



 


 
 
  
 
 


 


 

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Anaemia Among Women
 PREVALENCE OF ANAEMIA
IN PREGNANCY
Y Overall prevalence ² 40% of world·s population
Y Prevalence of anaemia is 3-
3-4 times higher in developing
countries. Average prevalence being 56%.
Y In industrialized countries approx 18% of women are
anaemic during pregnancy.
Y In India alone the prevalence of anaemia in pregnancy is as
high as 88% (W.H.O Global |atabase 1997).
 CLASSIFICATION OF
ANAEMIA IN PREGNANCY
ACQUIRE|:
Y Iron deficiency anaemia
Y Anaemia caused by blood loss
² Acute (APH)
² Chronic (Hook worm infestation, bleeding piles etc.)
Y Megaloblastic anaemia (Vitamin B12 and folic acid
deficiency)
Y Acquired hemolytic anaemia
Y Aplastic or hypo-
hypo-plastic anaemia
 CLASSIFICATION (Contd.)

HERI|ITARY:
Y Thalassemias
Y Sickle cell haemoglobinopathies
Y Other haemoglobinopathies
Y Hereditary hemolytic anaemias (RBC membrane defects,
spherocytosis)
 HAEMATOLOGICAL
CHANGES IN PREGNANCY
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 IRON |EFICIENCY
ANAEMIA
Y It is the commonest type of anaemia in pregnancy.
Y Food iron is made up of two pool
²Haem Iron Pool
²Non-
Non- Haem Iron Pool
Y Haem Iron Pool includes all food containing iron as
haem molecules, such as animal flesh and viscera. Its
absorption is 15-
15-30%, but it can increase to 50% in
iron deficiency state. Its absorption is usually not
affected by inhibitors.
 IRON |EFICIENCY
ANAEMIA (Contd.)
Y Non
Non--Haem Iron Pool includes cereals, vegetables, milk
and eggs. Its absorption can be increased by enhancers
and decreased by inhibitors.
Y Enhancers of absorption: Haem iron, proteins, meat,
ascorbic acid, ferrous iron, gastric acidity, alcohol, low
iron stores, increased erythropoietic activity.
Y Inhibitors of iron absorption: Phytates, calcium, tannins,
tea & coffee.
 CAUSES OF INCREASE|
PREVALENCE OF I.|.A
Y |ietary habits: Consumption of low-
low-bio availability diet
Y Food Fadism
Y |efective iron absorption due to intestinal infections,
hook worm infestation, amoebiasis, giardiasis.
Y Increased iron loss: Frequent pregnancies, menorrhagia,
hook worm infestation, chronic malaria, excessive
sweating, piles.
Y Repeated and closely spaced pregnancies and prolonged
period of lactation.
 CLINICAL FEATURES

Y SIGNS:
Y a)PALLOR b)GLOSSITIS c)ULCERATION IN MOUTH
c)SOFT SYSTOLIC MURMUR IN MITRAL AREA
d)CREPITATIONS AT BASE OF LUNG
SYMPTOMS:

LASITTUDEEAKNESSEXHAUSTIONANOREXIA
GIDDINESSDYSPNOEA
 IRON REQUIREMENT IN
PREGNANCY
Total iron requirement is 1000 mg.
Y Fetus and placenta -- 300 mg
Y Ń in red cell mass ² 500 mg
Y Basal loss ² 200 mg

Average requirement is 4-
4-6mg/day.
Y 2.5 mg/day in early pregnancy
Y 5.5 mg/day from 20-
20-32 weeks
Y 6-8 mg/day from 32 weeks onwards
 SEVERITY OF ANAEMIA

Y ICMR describes four grades of anaemia depending upon

the haemoglobin levels as shown:


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 EFFECTS OF ANAEMIA ON
PREGNANCY
Y Maternal effects:
ANTE NATAL INTRA NATAL POST NATAL
Poor weight gain |ysfunctional labour Puerperal Sepsis
Preterm labour Haemorrhage & shock Sub-
Sub-involution
Pre--eclampsia
Pre Cardiac failure Embolism
Abruptio placentae
Inter current infections
PROM
 EFFECTS OF ANAEMIA ON
PREGNANCY (Contd.)
Y Fetal effects:
² Risk of pre-
pre-maturity
² IUGR, LBW, poor apgar score
² |epleted iron store in neonates and anaemia in
infancy period
² High prevalence of failure to thrive and poor
intellectual development.
² Cardiovascular morbidity and mortality in adult lives.
 PREVENTION OF IRON
|EFICIENCY
Y Prophylaxis of non-
non-pregnant women ² 60 mg of elemental
iron daily for 3 months.
Y Iron supplementation during pregnancy.
² Routine iron supplementation is debatable in western
countries
² It has to be given in non-
non-industrialized countries
² W.H.O RECOMMEN|ATION: Universal oral iron
supplementation for pregnant women (60 mg of
elemental iron and 250 µg of folic acid) for 6 months
in pregnancy and additional of 3 months post-
post-partum
where the prevalence is more than 40%.
 PREVENTION OF IRON
|EFICIENCY (Contd.)
² MINISTRY OF HEALTH, GOVT. OF IN|IA
RECOMMEN|ATION: 100 mg of elemental iron with
500 µg of folic acid in second half of pregnancy for atleast
100 days. 2 injections of iron dextran (250 mg each) given
IMI at 4 weeks interval with TT injection.
Y Treatment of hook worm infestation
² Single albendazole (400 mg) or mebendazole (100 mg x B| x
3 days)
² Change in defecation habits and avoidance of walking bare
footed.
 PREVENTION OF IRON
|EFICIENCY (Contd.)
Y Improvement of dietary habits and improving bio
availability of food iron
Y Iron fortification of food.
 INVESTIGATIONS
Y Haemoglobin estimation
Y Peripheral blood smear ² microcytosis, hypochromia
anisocytosis, poykilocytosis and target cells
Y RBC indices ² ŅMCV, ŅMCH, ŅMCHC, MCV is the
most sensitive indicator
Y Ņ Serum ferritin ² first abnormal laboratory test
Y Ņ Transferrin saturation ² second to be affected
Y Ń FEP ² third test to become abnormal
Y Ń Serum transferrin receptor ² best indicator
 INVESTIGATIONS (Contd.)
Y Bone marrow examination ² no response to treatment after
4 weeks of therapy
² Aplastic anaemia
² |iagnosis of kala-
kala-azar
² Urine examination
² Stool examination ² for three consecutive days
² Other tests ² RFT, LFT, TSP A:G, chest x-x-ray,
sputum examination, etc.
² For response ² haemoglobin and PBS, reticulocyte
count
 MANAGEMENT OF IRON
|EFICIENCY ANAEMIA
AIM
Y To correct iron deficiency
Y To restore iron reserve
Y To correct associated complicating factor
CHOICE OF THERAPY
Y |epends on severity of anaemia
Y |uration of pregnancy
Y Associated complicating factor
 MANAGEMENT (Contd.)

GENERAL TREATMENT
Y |ietary advice
Y Treatment of associated complicating factor
IRON THERAPY
Y Oral
Y Parenteral
 ORAL IRON THERAPY

Y For women presents in mid trimester or early third

trimester
Y For treatment more than 180 mg of elemental iron/day is
required
Y To minimize side effects, start with low dose
Y Treatment is continued till blood picture becomes normal,
thereafter maintenance of one tablet daily for 3 months to
replenish iron stores
 IN|ICATIONS OF RESPONSE
TO THERAPY
Y Sense of well being
Y Improved outlook of patient
Y Increased appetite
Y Ń haemoglobin, haematocrit, reticulocytosis within 5-
5-10
days
If no significant clinical or haematological improvement
within 3 weeks, diagnostic re-
re-evaluation is needed.
 IN|ICATIONS OF RESPONSE
TO THERAPY (Contd.)
Y RATE OF IMPROVEMENT:
After a lapse of few days haemoglobin concentration is
expected to rise at a rate of 0.7 g/dl/week.
Y CAUSES OF FAILURE OF ORAL THERAPY
² Incorrect diagnosis
² Malabsorption syndrome
² Presence of chronic infection
² Continuous loss of iron
² Poor patient compliance
² Concomitant folate deficiency.
 PARENTRAL IRON THERAPY
IN|ICATIONS:
Y In tolerance to oral iron
Y Poor patient compliance
Y Unpredictable absorption
Y Patient near term
A|VANTAGE
Y No added advantage over oral iron except for certainty of
its administration.
 PARENTRAL IRON THERAPY
(Contd.)
PARENTERAL IRON THERAPY
YIntra muscular
YIntra venous
Two preparations ² Iron dextran ² IM/IV
Y Iron sorbitol citrate ² IM
IRON |EFICIT
Elemental iron needed (mg) = (Normal Hb ² Patient·s Hb) x
Weight (kg) x 2.21 + 1000
 PARENTRAL IRON THERAPY
(Contd.)
Simple method is to give 250 mg elemental iron for each gm
of haemoglobin below normal. Another 50 % is to be added
to replenish store.
Oral Iron should be stopped atleast 24 hrs prior to therapy
to avoid toxic reaction.
Iron injections are given daily or on alternate day by deep
IMI using ¶Z· technique.
I.V. ROUTE
Y Total dose in fusion (T|I) ² |ose calculated by same
formula
 PRE--REQUISITES FOR T|I:
PRE
Y Correct diagnosis of iron deficiency anaemia.
Y Adequate supervision in hospital setting.
Y Facility for management of anaphylactic reaction.
Sensitivity test done by 1ml test dose prior to infusion:
Y If no reaction iron dextran is diluted in normal saline or
5% dextrose and given over 4-4-6 hrs.
Y If total dose is more than 2500 mg infusion is given in 2
doses on consecutive days.
Y Look for reaction ² Chest pain, rigor chills, hypotension,
dyspnoea, haemolysis & anaphylactic reaction.
 IN|ICATION OF BLOO|
TRANSFUSION
Y Severe anaemia beyond 36 weeks
Y Refractory anaemia
Y To correct anaemia due to blood loss
Y Associated infection
 MEGALOBLASTIC ANAEMIA

Y DEARRANGEMENT IN RED CELL MATURATION

Y IMPAIRED DNA SYNTHESIS
Y EITHER VIT B R OR FOLIC ACID DEFICIENY
Y ADDISONIAN PERNICIOUS ANAEMIA DUE TO
DEFFECTIVE B R ABSORPTION
 FOLIC ACI| |EFICIENY

Y CAUSES:

Y INADEQUATE INTAKE
Y INCREASED DEMAND DUE TO:a)d maternal tissue
b)product of conception
Y DIMINISHED ABSORPTION
Y ABNORMAL DEMAND:a)twins b)infection
c)haemorrhagic states
Y FAILURE OF UTILISATION