Anaemia is common in pregnancy and can have serious consequences. The World Health Organization defines anaemia in pregnancy as a haemoglobin level below 11g/dL, though some territories use 10g/dL. Anaemia contributes to maternal mortality, especially in developing countries. Common causes include iron, folate, and vitamin B12 deficiencies, which can often be prevented with supplementation. Other causes include genetic conditions like sickle cell disease and thalassemia. Treatment depends on severity and may involve oral or intravenous iron, folic acid, vitamin B12, or blood transfusions in severe cases. Managing underlying conditions and nutritional deficiencies can help prevent anaemia in pregnancy.

1. ANAEMIA IN PREGNANCY

2. Anaemia in pregnancy
!
• The World Health Organization (1972) defines anaemia in
pregnancy as a haemoglobin concentration of less than
11.0g/dl.
!
• In Trinidad as well as in some other Caribbean territories,
a value of 10.0g/dl is used to define anaemia.

3. ❖ Anaemia in pregnancy is a major contributor to maternal
mortality, especially in developing countries.
!
!
❖Common types of anaemia in pregnancy are preventable with
appropriate dietary manipulation & supplementation.
!
!
❖ Anaemic patients are at a marked disadvantage due to:
1) Inability to withstand blood loss eg. Post Partum Haemorrhage
2)Increased risk of developing puerperal infection
3) Deep Venous Thrombosis

4. • Pregnancy is a hyperdynamic and hypervolaemic state.
!
• Plasma volume increases early in the 2nd trimester and
peaks at about 32-34 weeks gestation & may plateau in
the last 8 weeks.
!
• Expansion of about 1250-1500ml with multiple gestations.
Haematological Changes in
Pregnancy

5. • Red cell mass: increases by about 400-500ml (30%) in
pregnancy. This is as a result of accelerated
erythropoiesis.
!
!
• Reticulocyte count: Rises from about 16wks gestation
and peaks at 35weeks.
Haematological Changes in
Pregnancy

6. Haematological changes in Pregnancy
• A physiological anaemia results from the discrepancy
in increments of plasma volume and red cell mass.
!
• Occurs commonly at 28-32 weeks gestation.
!
• Oxygen delivery to the feto-placental unit is NOT
compromised at these levels of Hb owing to the
concurrent rise in maternal red cell 2,3-DPG.
!
• This rise facilitates oxygen transfer to the fetus.

7. Clinical Features of Anaemia
• SYMPTOMS
• Lethargy
• Shortness of breath
• Palpitations
• Chest pain
• Headaches
• Dizziness and fainting
!
• SIGNS
• Pallor
• Tachycardia
• Soft Ejection Systolic Murmur

8. Aetiology
➢ Nutritional Deficiencies
❑ Iron Deficiency Anaemia
❑ Folic Acid deficiency
❑ Vitamin B12 deficiency
!
➢ Physiological Anaemia
!
➢ Haemoglobinopathies
❑ Sickle Cell Anaemia
❑ Thalassaemia Syndrome
!
➢ Chronic disease such as renal failure
➢ Aplastic anaemia
➢ Haemolytic anaemia
➢ Leukemia/lymphoma

9. Iron Deficiency Anaemia
• Anaemia resulting from iron deficiency is
the commonest haematological problem in
pregnancy.
!
• Iron deficiency generally develops slowly
and is not clinically apparent until the
anaemia is severe even though functional
consequences already exist.

10. Iron Deficiency Anaemia
• The bulk of iron in the body is contained in the Hb of
circulating and developing red cells.
!
• This iron content is controlled by a limited variation in
absorption and NOT by excretion.
!
• The average diet contains 10-15mg of iron & 10% is
absorbed.
!
• Absorption occurring in the duodenum and proximal
jejunum and aided by gastric acid converting ferric
iron to the more soluble ferrous form.

11. Iron Deficiency Anaemia
• Iron absorption increases when iron
stores are depleted (e.g. when there is
a low ferritin level and high
concentration of unsaturated
transferrin)
!
• It also increases when there is
erythroid hyperplasia with a rapid iron
turnover.

12. Iron Deficiency Anaemia
• There are two distinct pathways of iron absorption
(one for organic and the other for Haem iron).
!
• Most foods contain the ferric form of iron which must
be converted to the ferrous form before absorption.

13. Iron Deficiency Anaemia
• Haem iron derived from haemoglobin and myoglobin
of animal origin is more effectively absorbed than
non-haem iron.
!
• Haem iron also promotes the absorption of inorganic
iron.
!
• Populations from underdeveloped parts of the world
subsist largely on non-haem iron hence the
prevalence of iron deficiency.

14. Iron Requirements in pregnancy
• Increased demand for iron in pregnancy is about 1000mg.
!
• During pregnancy, average requirement= 4mg/day, rising
from 2.5mg in early pregnancy to 6.6mg/day in the last
trimester.
!
• This demand arises from the increase in red cell mass and
requirements of the fetus and placenta.
!
• The fetus receives its iron from the maternal serum by
active transport across the placenta, mainly in the last
6wks of pregnancy.

15. Diagnosis: History
!
• Past gynaecological history: Fibroids may be the cause of
menorrhagia and depleted iron stores.
!
• Obstetric history: High parity especially with little spacing of births
or haemorrhage complicating pregnancy and multiple pregnancy
may decrease serum ferritin and predispose to anaemia.
!
• Chronic blood loss: e.g. Haemorrhoids or parasitic infection
(hookworms)
!
• Past history of gastric surgery or coeliac disease.
!
• Ascertain whether there has been good compliance with iron
supplements/dietary advice.

16. Investigations
BLOOD INVESTIGATIONS
!
• Haemoglobin level
• All blood indices (MCV,MCH,MCHC)
• Serum Ferritin (assesses iron stores)
• Serum iron
!
• Total Iron Binding Capacity (TIBC) à High
!
• Serum ferritin assesses iron stores. Ferritin is stable and not affected by
recent ingestion of iron. In the development of iron deficiency a low
serum ferritin is the first abnormal laboratory test.
!
• Serum iron even in combination with TIBC is unreliable as it fluctuates
widely and is affected by recent ingestion of iron and other factors such
as infection.
Low

17. Iron deficiency anaemia
!
Microcytic hypochromic picture on a blood film

18. Investigations
• Urine for microscopy and stools for occult blood and
ova, cysts and parasites should be included in lab
tests.
!
• At times, a bone marrow aspirate for iron stained with
Prussian blue is performed.
!
• NB- This is an invasive technique and is not usually
done.

19. Bone marrow aspirate showing Iron Deficiency
Anaemia

20. Prevention of Iron Deficiency
• Iron supplementation- considered for all pregnant
women.
!
• Prophylaxis with oral supplementation of 60-120mg/
day elemental iron should commence at 16weeks
gestation (when nausea and vomiting of early
pregnancy have subsided).
!
• Side effects of oral iron- Mild gastric upset &
constipation. Alleviated by increased fluid intake and
high fibre diet.

21. Management
• Treat underlying cause
• Treatment depends on severity, whether symptomatic
or not and on the period of gestation.
• All patients with severe anaemia (Hb ≤ 4g/dl)- urgent
admission to hospital. Risk of developing cardiac
failure. Transfuse with PRBC’s.
• Aim- Hb of at least 10g/dl at 40wks gestation.
• 1st week of treatment: No rise in Hb; only
reticulocytosis seen.
• End of 2nd week: Hb increases by approximately 1g/
dl/week.

22. Management
• Parenteral iron (e.g. Venofer ®) reserved for patients
intolerant of oral iron due to GI side effects & those
who are non-compliant with medication.
!
• Slightly faster rate of rise in Hb vs oral iron.
!
• Dose of Parenteral iron required to correct anaemia
• (“Normal” Hb of 13g/dl-Patient’s Hb) x 0.25

23. Folic Acid Deficiency
!
• What is Folic Acid?
!
• Water-soluble vitamin in the B-complex
group
!
• Folate-deficiency anaemia ?
• A decrease in red blood cells (anaemia) due
to a lack of folate

24. What does it do?
• Helps the body digest, utilize and synthesize proteins
!
• Helps in the production of red blood cells
!
• Helps synthesize DNA, Folic acid is needed for the
synthesis of purine DNA precursors.
!
• Aids tissue growth and cell function
!
• Stimulates the formation of digestive acids

25. Causes of Folic Acid Deficiency
• Pregnancy involves high DNA synthesis due to high
cell turnover, thus increasing folic acid demands.
!
• Folic acid is lost in the cooking process so dietary
means are not enough.
!
• Other causes of folic acid deficiency include:
anticonvulsants (phenytoin) and haemolytic anaemia.
!
• Folic acid deficiency leads to a macrocytic anaemia.

26. Megaloblastic Anaemia
• Decreased Hb
!
• Increased MCV (>95fl)
!
• Hypersegmented neutrophils
!
• Macrocytes
!
• Reduced red cell and serum folate
!
• Megaloblastic bone marrow changes
!
• White cells and platelets may be moderately reduced

27. Sources of Folic Acid
• Fortified cereal
• Bread, pasta & rice
• Beans
• Legumes, lentils
• Green Vegetables
• Asparagus, kale, spinach
• Fruits
• Strawberry, orange

28. Clinical Features of Folic Acid Deficiency
• Pallor with mild icterus
• Glossitis
• Angular stomatitis
• Neural Tube Deficiencies (NTDs)
Spina bifida
Anencephaly

29. Exams and Tests
• Complete blood count (CBC)
• Red blood cell folate level
• Rarely, a bone marrow examination
may be done.

30. Treatment of Folic Acid Deficiency Anaemia
• Prophylaxis with folic acid.
!
• Mandatory in grand multiparas, patients with previous
abruptio placentae and multiple pregnancy.
!
• 200 – 300mcg daily in all pregnant women.
!
• If megaloblastic haematopoiesis is established,
treatment with folic acid 5mg daily shoud be
commenced immediately and continued for several
weeks after delivery.

31. Prevention
• Eating plenty of folate rich foods can help prevent this
condition.
!
• Experts recommend that women take 400
micrograms (mcg) of folic acid every day before you
get pregnant through the first 3 months of pregnancy.

32. Vitamin B12 Deficiency
!
What is it?
• VB12 is a water soluble vitamin that is involved in
normal functioning of living cells and brain function
!
• It is also called cobalamin
!
• It is closely related of folic acid (VB9) with respect to the
synthesis of DNA, fatty acids and energy production.
!
• Fungi, plants and animals cannot produce B12. The
only source of B12 is that from animal derived products,
namely meat, eggs and dairy products.

33. Causes of B12 deficiency in Pregnancy
• B12 deficiency is uncommon in pregnancy.
!
• Diet: Most prevalent among strict vegetarians who do
not eat any animal derived foods.
!
• Pernicious anaemia (PA) : Auto antibodies that attack
the gastric parietal cells which secrete Intrinsic
Factor. IF is essential in the absorption of Vit B12 in
the terminal ileum. However, PA is most common in
women age 60, and rare in the reproductive years.

34. Diagnosis
• Diagnosis is primarily clinical plus serum B12 levels.
!
• Clinical symptoms are typical of anemia such as
fatigue, pale skin, pale mucus membranes, dyspnoea
and palpitations.
!
• Severe deficiency can also cause neurological
symptoms such as paraesthesia, numbness, cognitive
changes or visual disturbance.
!
• Psychological symptoms can include irritability,
psychosis and dementia.

35. Treatment
• The normal amount of B12 in adults is 2-5mg, which
0.1% is lost every day mainly via bile.
!
• The recommended intake of B12 in pregnancy is 3.0
mg per day.
!
• Treatment is by weekly IM of cyanocobalamin.
!
• Cyancobalamin is a fermented derived source of B12
that is used to treat various causes of B12 deficiency,
such as diet, pernicious anaemia and ilectomy.

36. Haemoglobinopathies
Inherited genetic defects of haemoglobin,
resulting from :
!
• 1. Impaired globin synthesis –
Thalassemia syndromes.
or
• 2. Structural abnormality of globin –
Haemoglobin variants such as Sickle
Cell Disease

37. Thalassaemia
!
!
Heterogeneous group of inherited
disorders of haemoglobin synthesis,
resulting from a reduced rate of
production of one or more of the globin
chains of haemoglobin.

39. Beta thalassaemia major
• Transfusion dependent (2-5wks)
• Iron Chelation
• Infertility
• During pregnancy, Hb levels are kept near 10g/dL
• Desferoxamine is usually D/C because its safety in
pregnancy has not been established.
• Increased risk of complications during pregnancy
• Increased risk of CPD (bone deformities)

40. β thalassemia trait
• Hb ≈ 1 to 2 grams below normal
• Generally microcytic (MCV<75 fl ) and
hypochromic (MCH<26 pg)
• Reticulocytes: normal or mildly elevated
• RDW generally normal (unlike Fe deficiency)
• Target cells on blood film
Confirmed by Hb electrophoresis-
HbA2 elevated (3.5-7%) +/-↑HbF
• Coexisting iron deficiency may mask HbA2
elevation

42. Approach to patients with β thalassemia trait
Parenteral iron should NEVER be used
!
• Serum Ferritin HIGH Withhold Oral Fe
Folate supplementation
• Serum Ferritin LOW Oral Fe in antenatal period
Folate supplementation
!
• β-thalassemia minor patients have a favourable
pregnancy outcome although there is a possible risk
of oligohydramnios and IUGR

43. α thalassemia
4 α globin genes, 2 copies on each
(chromosome 16)
!
• 1 gene deletion- silent carrier
• 2 gene deletion- α thal trait
• 3 gene deletion- Hb H disease
• 4 gene deletion- Hb Bart’s hydrops fetalis:
lethal in utero

44. HbH disease
• Blood transfusion required:
Severe anaemia
• Folic acid supplementation :
Increased risk of neural tube defects

45. Sickle Cell Disease
A group of conditions in which the pathology may be attributed
to the presence of sickle haemoglobin.
!
Four principle genotypes:
!
✓ SS disease
✓ SC disease
✓ S-thalassemia
✓ Sickle cell trait
!
!
!
!
• Normal Hb level in SS patient 6.0-8.0g/dL

46. Tests for Sickle Hb
Routine procedure in antenatal clinic at
booking;
• Sickle Test
• Gel Electrophoresis

47. Peripheral Blood Film
• Peripheral blood films reveal – anisocytosis,
poikilocytosis, macrocytes, large numbers of
nucleated red cells and hypersegmented neutrophils

48. COMPLICATIONS OF SCD IN PREGNANCY
• ↓fertility potential due to late menarche, less sexual exposure,
anaemia and chronic ill health
• ↑ risk of spontaneous miscarriage
• ↑ incidence of infection especially pyelonephritis,
pneumococcal pneumonia, possibly salmonella osteomyelitis
and puerperal sepsis.
• ↑ risk of thrombo-embolism
• ↑ incidence of pre-eclampsia
• ↑ risk of abruptio placentae
• Preterm labour and IUGR more common
• Acute and chronic fetal distress
• ↑risk of stillbirth and higher perinatal mortality rate
• ↑Maternal mortality rate (less common because of improved
care)
• Painful crises are more common

49. Painful Crises
➢ Pain felt in extremities, back, abdomen, or chest.
Associated with fever, and passage of dark or red urine.
!
➢ Precipitated by;
!
✓ Infection, especially in urinary tract and respiratory tract
✓ Pyrexia
✓ Hypothermia
✓ Acidosis and hypoxia
✓ Dehydration
✓ Emotional stress
✓ High altitude
✓ Smoking
✓ Excessive exercise
✓ Labour

50. Management of a painful crisis
➢Admit to antenatal ward
➢Bed rest with O₂ (if SpO2 <95%)
➢Reassurance
➢Sputum & Urine investigations for infection.
➢Rehydration: Oral as well as IVF w/ NS or RL
➢Analgesia
➢Limited exchange transfusion to reduce HbS
concentration to <30 %
➢Broad spectrum antibiotics
➢If period of gestation is >30wks, NST to determine
fetal well being

51. Acute anaemia
• May arise from aplastic crisis and less commonly
from acute splenic sequestration (mainly seen in 3rd
trimester)
!
• Absence of reticulocytes and rapidly falling Hb level
!
• Clinical features: listlessness, pale MM, URTI
!
• Treatment: blood transfusion
!
• Spontaneous recovery of marrow within 5-10days

52. Acute Chest Syndrome
• Sudden onset of pleuritic chest pain, dyspnoea
and tachypnoea consistent w/ either pneumonia
or PE, occurs commonly in pregnancy.
!
• During a painful crisis necrotic bone marrow, fat
and even spicules of bone may embolise to
small vessels in lung.
!
• Treatment: supportive therapy with blood
transfusion, O2, heparin

54. Management of sickle cell disease in pregnancy
• Early booking to antenatal clinic
!
• Joint care by obstetrician and haematologist
!
• Folic acid and Fe supplementation
!
• Repeated Hb and RFT assessment and determination of HbS
concentration
!
• Consider partial exchange transfusion with HbA to keep level of
HbS <30%
!
• Fortnightly midstream urine for M/C/S

55. Management of sickle cell disease in
pregnancy
!
• Antenatal diagnosis—chorionic villus sampling,
amniocentesis or fetal blood assessment (cordocentesis)

56. Management of sickle cell disease in
pregnancy
• Early U/S for accurate dating of
pregnancy
!
• Antenatal visits every 2 wks up to 28 wks
gestation, and then weekly until delivery
!
• Regular monitoring of BP and urinalysis
for proteinuria which ensures early
diagnosis of pre-eclampsia

57. Management of sickle cell disease in pregnancy
• Pneumococcal vaccine or penicillin V
administered in pregnancy (prophylaxis)
!
• Assessment of fetal well being with fetal kick
charts, biophysical methods (NST) in 3rd trimester
!
• Monitoring of fetal growth with maternal weight,
serial symphysio-fundal ht & If IUGR suspected,
U/S measurements of biparietal diameter,
abdominal circumference, and femur length.

58. Management of sickle cell disease in
pregnancy
Admission to antenatal ward for:
!
• Crises
• Pre eclampsia
• IUGR/preterm labour
• Abruptio placentae
• Fetal distress
• Pyelonephritis
• Thromboembolism

59. Time and mode of delivery
• SS disease is considered to be an indication for induction of labour at 38-40wks
gestation
!
• Caesarean section is required for obstetric indications and sometimes for pelvic
deformity
!
• Intrapartum Management :
✓ O₂
✓ IVF
✓ Analgesia
✓ active Mx of 1st stage of labour
✓ continuous CTG monitoring
✓ in 2nd stage ,an episiotomy and possible assisted delivery with outlet forceps
!
• Antibiotics for postpartum pyrexia (from endometritis). Encourage breastfeeding
!
• Neonatal diagnosis can be made with gel electrophoresis of cord blood.d

60. Contraception
• Sterilization should be considered as a
permanent form of contraception especially
when no further pregnancies are required.
!
• Medroxyprogesterone acetate
!
• Progesterone only pill
!
• IUCD is contraindicated