This document discusses anaemia complicating pregnancy. It defines anaemia as an insufficient hemoglobin level to carry out oxygen requirements to tissues. The World Health Organization defines anaemia in pregnancy as a hemoglobin level of less than 11 gm%. Iron deficiency is the most common type of nutritional anaemia seen in pregnancy. Left untreated, anaemia can lead to complications for both the mother and fetus such as increased risk of maternal and perinatal mortality. Treatment involves oral or parental iron supplementation depending on the severity of the anaemia.

1. ANAEMIA COMPLICATING
PREGNANCY
DR:HUSSEIN H AKL
O&G SPECIALIST
HOSPITAL SEGAMAT

2. Definition
Anemia - insufficient Hb to carry out O2 requirement
to the tissues.
WHO definition : Hb conc. 11 gm %
CDC definition : Hb conc. < 11gm % in 1st and 3rd
trimesters and < 10.5 gm% in 2nd trimester
For developing countries : cut off level suggested is
10 gm %
- WHO technical report Series no. 405, Geneva 1968
Centre for disease control, MMWR 1989;38:400-4

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. Degree Hb% Haematocrit (%)
Moderate 7-10.9 24-37%
Severe 4-6.9 13-23%
Very Severe <4 <13%
WHO Classification of Anaemia

5. Magnitude of Problem
Globally, is about 30 %
In developing countries &
India, incidence is around
40 – 90%.
Responsible for 40% of
maternal deaths in third world
countries.
Important cause of direct and
indirect maternal deaths
- Vitere FE Adv Exp Med Biol 1994;352:127

6. Infection
Lack of
Concentration
Weakness
Irritability
Palpitation
Fatigue
Dizziness
Symptoms

7. Clinical Features
Pallor of skin
And m/m
Edema
Platynychia
Koilonychia
Glossitis
Stomatitis
Tachycardia
Soft ejection
systolic
murmur
Signs

9. IRON DEFICIENCY ANEMIA
GENERAL ANEMIA’S SYMPTOMS:
•FATIGABILITY
•DIZZENES
•HEADACHE
•SCOTOMAS
•IRRITABILITY
•ROARING
•PALPITATION

10. pallor

11. Conjunctival Pallor

12. Koilonychia

14. CHARACTERISTICS
SYMPTOMS
•GLOSSITIS, STOMATITIS
• DYSPHAGIA ( Plummer-Vinson syndrome)
•ATROPHIC GASTRITIS
•DRY, PALE SKIN
•SPOON SHAPED NAILS,
KOILONYCHIA,
•BLUE SCLERAE
•HAIR LOSS
•PICA (APETITE FOR NON FOOD

15. Physiological
Pathological
Causes of Anaemia
Nutritional
Haemorrhagic
Haemolytic

16. 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

18. Iron Requirement
Iron Absorption
1
Amount of iron in the
body
Iron Loss
Skin
Urine
Feces
Menstruation
1-2mg/d
20-30mg/c

19. 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

21. Criteria for Physiologic Anemia
Hb: 10gm%
RBC: 3.2 million/mm3
PCV: 30%
Peripheral smear showing normal morphology of
RBC with central pallor

23. Significance of Hypervolemia
1. To meet the demands of the enlarged
uterus with its greatly hypertrophied
vascular system.
2. To protect the mother, and in turn the
fetus, against the deleterious effects of
impaired venous return in the supine and
erect positions.
3. To safeguard the mother against the
adverse effects of blood loss associated with
parturition.

24. Normal hemoglobin by gestational age in pregnant
women taking iron supplement
12 wks 12.2 [11.0-13.4]
24wks 11.6 [10.6-12.8]
40 wks 12.6 [11.2-13.6]

25. Early
Pregnancy
2.5 mg / day
32 to 40
weeks
6.8 mg / day
TOTAL
800 – 1000 mg
20 to 32
weeks
5.5 mg / day
Iron Requirement During Pregnancy

26. 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

27. Hb 13.5 – 14 gm %
R.B.C. 4.5 – 4.7 million/cu mm
Serum Iron 50 – 150 μg / dL
TIBC 300 – 360 μg / dL
Transferrin saturation 25 – 50 %
S. Ferritin level 30 μg / Lit
Red Cell protoporphyrin 30 μg / dL
Erythropoietin 15.20 U / Lit
MCV 76 – 100 fL
MCH 27 – 33 pg
MCHC 33.37 gm / dL
PCV 32 – 40 %
Normal Levels

28. 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.

30. IRON DEFICIENCY ANEMIA
ETIOLOGY:
–CHRONIC BLEEDING
•MENORRHAGIA
•PEPTIC ULCER
•STOMACH CANCER
•ULCERATIVE COLITIS
•INTESTINAL CANCER
•HAEMORRHOIDS

31. CLINICAL FEATURES
Symptoms usually in severe anaemia
- Fatigue
- Giddiness
- Breathlessness

32. EFFECTS OF ANAEMA IN
PREGNANCY
. Mother :
– High output- due to inadequate tissue
oxygenation, increase cardiac failure (more
likely if reqirement for excessive blood flow )
– PPH
– Predisposes to infection
– Risk of thrombo-embolism
– Delayed general physical recovery esp after c.
section

33. Fetus: . IUGR
. Preterm birth
. LBW
. Depleted Fe store
. Delayed Cognitive function.

34. IUGR
IUD ABOR
TION
CCF
INFECTION
PRETERM
LABOUR
PIH
Medical
Disorder
Complications - Pregnancy

35. Instrumental
delivery
PPH
Foetal
DistressCCF
MATERNAL
PERINATAL
Morbidity
Mortality
Complications - Labour

36. Laboratory Diagnosis of Anaemia
IDA Thalassemia Chronic Diseases
Serum Iron Decreased Normal / Increased Decreased
TIBC Increased Normal Decreased or N
Transferrin
Saturation
Decreased N or Increased N or Decreased
Serum Ferritin Decreased N or Increased N
Marrow Iron Decreased /
absent
N or Increased N
Therapeutic test with
oral iron
Rise in Hb No rise in Hb No rise

37. 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

38. 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.

43. BLOOD AND
BONE MARROW SMEAR
BLOOD:
microcytosis, hipochromia, anisocytosis
poikilocytosis
BONE MARROW
high cellularity
mild to moderate erythroid hyperplasia (25-35%;
N 16 – 18%)
polychromatic and pyknotic cytoplasm of
erythroblasts is vacuolated and irregular in
outline (micronormoblastic erythropoiesis)
absence of stainable iron

44. 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

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

46. National Nutrition Anaemia Prophylaxis
Programme (NNAPP 1971 - 72)
Anaemia continues – Major health problem
Nutritional Anaemia :
Major Health Problems
FS + FA
Pregnancy
Lactating mothers
Family planning acceptors
Children – 1 to 11 years

47. Reason For Increased
Incidence Of Anemia
Poor pre-pregnancy iron balance due to –
untreated systemic diseases & menstrual
disorders
Improper supplementation of iron in pregnancy
( late registration and poor follow up)
Repeated childbearing
Lack of awareness and illiteracy

48. Low socioeconomic status and poor hygiene
Chronic malnutrition
Poor availability of iron due to predominantly
veg diet, diet low in calories but rich in phytates.
Food and religious taboos
GI infections and infestations
(e.g. Kala azar, worm infestations)
Reason For Increased
Incidence Of Anemia

49. Management Options
Pre – pregnancy :
Treat the cause before conception
Pre-pregnancy balanced diet, education
and health support.
Build up iron stores during adolescent
phase

50. Oral Iron
Blood
transfusionParenteral
Injectable Iron
Human Recombinant
Erythropoietin
Modalities of Management

51. 100 mg elemental Iron ------- ↑ 0.18 gm % day
Iron stores poor
-ve
Iron absorption
↓ Bioavailability
of Iron
Phosphate
phytate
Worm
infestation
Oral Iron

52. Oral Iron Therapy
Ideal dose – 100mg per day (prophylactic)
Ferrous gluconate, ferrous fumarate, ferrous
succinate, ferrous sulphate, ferrous ascorbate citrate
Rise in Hb – 0.8 gm / dl / week
Side effects -G I upset most common
Pt. compliance not guaranteed
Ineffective in pts with worm infestations
Inconclusive evidence on benefit of controlled release
Iron preparation

53. Iron salts are dissociated into bivalent or trivalent iron salts
Diffuses as free iron ions through the upper part of the
gastrointestinal mucosa
Taken up by transferrin and incorporated into ferritin.
For binding to ferritin and transferrin ferrous iron has to be
converted into ferric iron by oxidation
Highly reactive free radicals are produced during this process
All ionic iron including carbonyl iron are absorbed similarly
• Borbolla JR. Cicero RE, Dibilox MM, Sotres RD et al.. Rev Mex Pediatr 2000; 67(2): 63-67
• Heubers KA, Brittenham GM, Csiba E, Finch CA. J Lab Clin Med 1986 ; 108 ; 473-8.
Absorption of Ferrous Salts
Uncontrolled Passive Absorption

54. Fe+2
Fe+2
Fe+2Fe+2
Dissociation
Passive diffusion
Fe+2
Fe+2
Fe+3
Fe+2
Fe+3
Gut Lumen Mucosal Cell Blood
Ferritin
Iron
salts
Fe+3
Free
Radical
Fe+2
Fe+2
Fe+2
Fe+2
Fe+2
Fe+2
Fe+2
Fe+3
Free
Radical
Transferrin
Incorporation into
Hb

55. ↑ Hb – 0.21 gm %
Fractionated Irondextran
[Iron hydroxide dextran complex]
Parenteral Therapy
100 mg elemental
Iron
Anaphylactic
reaction
Anaphylactic
reaction
I.M. I.V.

56. Parenteral Therapy :
Traditional Indications
Intolerance to oral iron
Poor compliance to oral iron
Gastrointestinal disorders
Malabsorption syndromes
Rapid blood loss

57. IRON DEFICIENCY ANEMIA
CURE
PARENTERAL IRON SUBSTITUTION
Bad oral iron tolerance (nausea, diarrhoea)
Negative oral iron absorption test
Necessity of quick management (CHD, CHF)
50 - 100 mg daily
I.v only in hospital (risk of anaphilactic shock)
I.m in outpatient department
iron to be injected (mg) = (15 - Hb/g%/) x body
weight (kg) x 3
TDI(in mg)=2.3xWxD+500

58. Inability to maintain iron balance
(haemodialysis)
Patient donating large amount of blood
for auto-transfusion programme
? Pregnant women with severe IDA,
presenting late in pregnancy
Parenteral Therapy :
Traditional Indications

59. The
World Health Organisation
states…
‘transfusion should be
prescribed ONLY for conditions
for which there is NO OTHER
TREATMENT’

60. FOLATE DEFICIENCY ANAEMIA
At cellular level
Folic acid reduced to Dihydrofolicacid then
Tetrahydro-folicacid . (THF) c 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.

62. 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.

63. 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.

64. 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.

65. 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.

66. Diagnosis of Folate Deficiency
Anemia (FDA)
Special considerations in diagnosis
• FDA is suspected when the expected response
to adequate iron therapy is not achieved
• Macrocytosis can occur in pregnancy in absence
of FDA
• If FDA + IDA present, it will be masked by IDA
• Definitive diagnosis – Bone marrow aspirate

67. Megaloblastic Anemia
- Diagnostic Problems
HB estimation
Peripheral smear
MCV estimation
Serum folate
Red cell folate
FIGLU estimations
Marrow aspirate

68. Management of FDA
Strong case for routine prophylaxis
Prophylaxis with anti convulsants
Continue routine oral therapy for
hemolytic anaemia
Parenteral therapy for severe deficiency

69. Worm Infestations
Common cause of anaemia in developing countries
Most common – hookworm infestation, Round
worm, whip worm, etc.
Oral iron therapy becomes ineffective
Treatment by antihelminthics is a must
Treatment
Mebendazole : 100mg twice daily for three days
Pyrantel pamoate : 10mg / kg in single dose.
Albendazole : 400mg once a day for three days

70. Hemoglobinopathies
A collective term for the inherited disorders
of Hb synthesis
Disorders of globin synthesis e.g.
Thalassemia
Structural Hb variants e.g. Sickle cell
anemia, HbC

71. 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.

72. HAEMOGLOBINOPATHIES
DEFINITION:
Inherited disorders of haemoglobin.
Defect may be in:
- Globin chain synthesis------thalassemia.
- 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)

73. 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

74. Thalassemia
Genetic disorders; lack or sed synthesis of globin
chains
Two types : & thalassemia
chains encoded by 2 pairs of genes on
chromosome 16
chains encoded by single pair of genes on
chromosome 11
thalassemia more common and presents as either
(major) or + (minor)

75. Beta thalassemia 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.

76. Beta Thalassemia 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.

77. Beta Thalassaemia 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 thalassaemia trait.
HbH disease.
Alpha thalassaemia major.

78. Diagnosis of Thalassemia
Hb estimations
Peripheral smear
sed MCV
sed MCH
HbA2 ( 2 2)

79. Diagnostic Strategy for Thalassemias
Hb Electrophoresis + CBC
Abnormal band
Normal No action
MCV
MCH
Quantitative Hb
electrophoresis
Raised Hb A2
B Thalassemia
Normal
sed Examine partners blood
? X
Thalassemia
DNA analysis
for x gene
defects

80. 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.

81. 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

82. Sickle Cell Disease
Structural Hb variant
Exists in homo & heterozygous
forms
Under hypoxic conditions, HbS
polymerizes, gels or crystallizes.
hemolysis of cells, &
thrombosis of vessels in
various organs
In long standing cases,
multiple organ damage.

83. SCD
Diagnosis:
- Hb. Electrophoresis
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

85. 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

86. Take Home Message
Anaemia although preventable is a global problem
Anaemia still is the commonest cause of maternal mortality
and morbidity in spite of easy diagnosis and treatment
Anaemia can be due to a number of causes,
including certain diseases or a shortage of iron, folic
acid or Vitamin B12.
The most common cause of anemia in pregnancy is
iron deficiency.
Iron therapy is best given orally

87. The youth need to be educated about diet,
sanitation and personal hygiene
Hookworm infestation should be treated
Pregnant women should be given Iron and
folate supplements
Take Home Message

88. Thank You
Egypt