ANAEMIA IN PREGNANCY

BY

Dr. Dickenns Omanga

ANAEMIA IN PREGNANCY
Commonest

medical disorder.
High incidence in underdeveloped countries
Increased Maternal morbidity & mortality
Increased perinatal mortality

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
Severe anaemia-------- < 7gm /dl
Very severe anaemia-- < 4gm/dl

ETIOLOGY
There are 3 main causes:
1- RBC production:
. Fe deficiency
. Folic acid deficiency
. Vitamin B12 deficiency
2- RBC destruction: Sickle cell, tumors, etc
3- RBC loss: Hrrge, helminths, etc
***90% anemia in pregnancy is due to Fe deficiency

Physiological changes in
pregnancy
Plasma volume
by 50% (by 34weeks)
But RBC mass by only 25%
Results in haemodilution :
Hb
Haematocrit
RBC count
No change in MCV or MCH
2-3 fold increase in Fe requirement.
10-20 Fold increase in folate requirement

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
- Hodgkins disease
- Paroxysmal nocturnal haemoglobinurea

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
- Dizziness
- Breathlessness

EFFECTS OF ANAEMIA IN PREGNANCY

Mother :
High output Cardiac failure (more likely if preeclampsia
present.)
PPH
Predisposes to infection
Risk of thrombo-embolism
Delayed general physical recovery esp after c. section

Fetus:
IUGR
Preterm birth
LBW
Delayed Cognitive function.

INVESTIGATIONS (for Fe
Deficiency Anaemia)
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 : Transferrin in nonpregnant state is 33% saturated with iron.When
serum iron level falls, <15% saturated. By fall in
saturation, the TIBC is INCREASED.

Serum

ferritin: In healthy adults ferritin circulates 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 protein that binds
transferrin iron and transfer it to cell
interior. Increased in iron def. anemia.
Bone marrow examination.
RFTs/LFTs.
Urine for hematuria.
Stool examination for ova, cysts and occult
blood.

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 transfusion
Choice of method:
It depends on three main factors:
Severity of the anaemia
Gestational Age
Presence of additional risk factor

MANAGEMENT
Recommended

supplementation for non-anaemiac

30 - 60mg /day of elemental iron
Anaemic 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

MANAGEMENT
Severe

anaemia: (Hb < 8gm/dl)- preferably

parenteral therapy in the form of I/M or I/V iron
- I/M : (Iron sorbitol) with Z-track technique
- I/V : (iron sucrose)
Iron needed =
(Normal Hb Pt. Hb)* Wt in Kg*2.21+1000)

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 Dihydrofolic acid then
Tetrahydrofolic acid (THF). THF is required for cell
growth & division.
Active tissue reproduction & growth are dependent
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, thalasemias, 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 Family 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 pg/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%.

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 genes, 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)

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

Beta thallassemia minor

Beta

Thalassemia 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.

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.

Severe anaemia.
Diagnosed in paediatric age group.
Management is blood transfusion.
ALPHA THALASSAEMIA:
Both heterozygous & homozygous forms exist.
Alpha thalassemia trait.

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)

Sickling

crises frequently occurs in pregnancy,

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

SCD
Diagnosis:

- Hb. Electrophoresis
- Sickling test is screening test
Management:
- No curative treatment.
- Only symptomatic
- Well hydration, effective analgesia, prophylactic
antibiotics, O2 inhalation, folic acid, oral iron
supplement (I/V iron is C/I), blood transfusion

Management During Labour

Comfortable

Position
Adequate analgesia
O2 inhalation
Low threshold of assisted delivery
Avoid ergometrine
Prophylactic antibiotics
Continue iron & folate therapy for 3 months after
delivery
Appropriate contraceptive advice

GENERAL NURSING CONSIDERATIONS FOR

PREGNANT CLIENTS
Assess

nutritional intake and status

Assess for fatigue, pallor, sore tongue, anorexia,
N&V, stomatitis, signs of infection, severe pains
(vaso-oclusive crisis)
Observe and monitor hemat results (Hb)
Encourage diet rich in Iron & Folate (Green leafy
veges, fish, meat, legumes)
Teach food preparation methods that conserve Fe &
folate (e.g steaming)

Contd
Encourage

taking foods high in Vit C for Iron

absorption e.g. fruits
Emphasize high fibre diet and fluids to avoid
constipation from Iron supplements
Emphasize good hygiene to avoid UTIs
Teach client to watch out for signs of preterm
labour
Observe and monitor fetus
Rest and emotional support