BY
Dr. Sonal Dewangan
 What is Anaemia ?
Anaemia is defined as reduction in
circulating haemoglobin mass below the critical
level.
 The normal haemoglobin (Hb) is 12-14 gm%.
 WHO has accepted up to 11 gm% as the
normal haemoglobin level in pregnancy.
 Therefore any haemoglobin level below 11gm
in pregnancy should be considered as
anaemia
 Anaemia in pregnancy is present in very
high percentage of pregnant women in
India.
 Exact data is not available about the prevalence
of nutritional anaemia. However according to
WHO, the prevalence of Anaemia in pregnancy
in south East Asia is around 56 %.
 In India incidence of anaemia pregnancy
has been noted as high as 40-80%.
Total iron requirement is 1000 mg.
 Fetus and placenta -- 300 mg
 ↑ in red cell mass – 500 mg
 Basal loss – 200 mg
Average requirement is 4-6mg/day.
 2.5 mg/day in early pregnancy
 5.5 mg/day from 20-32 weeks
 6-8 mg/day from 32 weeks
onwards
 Anaemia is often classified
as Mild degree (9-11 gm %)
Moderate (7-9 gms %)
Severe (4-7 gm %)
Very severe (<4gm %)
 It is also classified according to
Haematocrit (PCV) %.
Antenatal Period
-Poor weight
gain
-Preterm labour
-PIH
-Placenta Previa
-PROM
Postnatal Period
-Postnatal
sepsis
-Sub involution
-Embolism
Intranatal Period
-Dysfunctional
Labour
-Intranatal
-Hemorrhage
-Shock
-Cardiac Failure
-Anaethesia risk
MATERNAL COMPLICATIONS
•
•
•
•
•
Prematurity
Low birth weight
Poor apgar score
Foetal distress
Neonatal
Anaemia
FETAL AND NEONATAL
COMPLICATIONS
 Physiological
 Nutritional: Iron deficiency
 Folate &/or Vit B12
deficiency Dimorphic
 Hemorrhagic: Acute or Chronic
 Hemoglobinopathies
 Hemolytic: Congenital or acquired
 Aplastic anaemia
Symptoms
 Fatigue
 Loss of
appetite
 Digestive
upset
 Dyspnoea
 Palpitation
Signs
Pallor
Pale nails
Koilonychias
Pale Tongue
Severe Case -
Oedema
• CBC
• Pheripheral Smear –
Hypochromic
Microcytosis
Poikilocytosis
Anisocytosis
• MCV, MCH, MCHC
• TIBC
• Serum Iron
• Serum Ferritin
• Free erythrocyte
protoporphyrin
• Bone marrow examination
• Urine examination
• Stool examination
• Serum protein
 Serum Folate
 RBC folate
 Serum Vit B12
 Serum Bilirubin
 Coombs test
 HB electrophoresis
 NESTROF test
 Red cell osmotic
fragility
 Routine screening for anaemia for
adolescent girls from school days
 Encouraging iron rich foods
 Fortification of widely consumed food with
iron
 Providing iron supplementation from school
days
 Annual screening for those with risk factors
 PROPHYLAXIS OF NON-PREGNANT WOMEN – 60 MG
OF ELEMENTAL IRON DAILY FOR 3 MONTHS.
 Iron supplementation during pregnancy.
 Routine iron supplementationis debatable in
western countries
 It has to be given in non-industrialized countries
 W.H.O RECOMMENDATION: Universal oral iron
supplementation for pregnant women(60 mg of
elemental iron and400 µg of folic acid) for 6 months in
pregnancy and additional of 3 months post-partum
where the prevalence is morethan 40%.
 MINISTRY OF HEALTH, GOVT. OF INDIA
RECOMMENDATION: [CSSM] 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.
 Treatment of hook worm infestation
 Single albendazole (400 mg)or mebendazole (100 mg x BD x
3days)
 Change in defecation habits and avoidance of walking b
a
r
e
footed.
PULSES, CEREALS, JAGGERY, BEETROOT, GREEN LEAFY
VEGETABLES,MEAT,LIVER,EGG,FISH,LEGUMES,DRY
BEANS

MOTHER
 PREGNANCY-
1. Cardiac failure at 30-34 wks of
pregnancy
2. Increased susceptibility to infection
3. Preterm labour
4. Preeclampsia
 LABOUR-
5. Uterine inertia
6. Post partum haemorrhage
7. Cardiac failure
8. shock
 Puerperium
1. Cardiac failure
2. Puerperal sepsis
3. Subinvolution
4. Failing lactation
5. Chronic ill health,backache
 FETUS&NEONATE
6. Prematurity
7. IUGR
8. Increased perinatal death
9. Decreased iron stores in
neonate
 ORAL IRON THERAPY
1. Safe,inexpensive and effective way
to administer iron
2. National nutritional anemia prophylaxis
program suggest 60 milligrams of
elemental iron and 500 micrograms of
folic acid daily
3. However it is suggested that 120 milligram
of elemental iron and 1 milligram of
folicacid are the optimum daily dose
needed
SALT TABLET ELEMENTAL
IRON
Ferrous sulfate 200mg 60mg[30%]
Ferrous fumarate 200mg 66mg[33%]
Ferrous gluconate 320mg 36mg[12%]
Ferrous succinate 100mg 35mg[35%]
Ferric
ammonium
citrate
125mg 25mg[17-22%]
Ferrous ascorbate ------ 100mg
Carbonyl iron ------- 90mg
Sodium feredetate ------- 231mg
Hb preparation 2.1g [0.33%]
 SIDE EFFECTS OF ORAL IRON
A. UPPER GI TRACT
Nausea,gastric discomfort,loss of
apetite,staining of teeth
A. LOWER GI TRACT
Constipation,diarrhoea,flatulance
 PARENTRAL IRON THERAPY
 Preparation
Iron sucrose-Imax S[100mg/5ml],orofer
s[50mg
/2.5ml]
Iron sorbital citric acid complex-
jectocos Iron dextran-imferon
 Intramuscular iron
1. 0.5ml test dose should be given
2. 75/100mg/day is given daily on alternate
days
3. Given deep Im by Z-techniue to prevent
skin staining
4. Side effects-
painful,discolouration,injection abscess
 INTRAVENOUS IRON
1. Formula-0.66*% deficit of Hb*wt in kg=mg of
iron
2. Total dose in mg/50=ml of imferon
3. Total dose is given in normal saline
 COMPLICATION
Local-thrombophlebitis at IV site
Systemic-malaise,fever,arthralgia,utricaria
lymphadenopathy
 BLOOD TRANFUSION
1. Indicated insevere anemia at any
GA,moderate anemia beyond 36wks and
when there is a failure of response to iron
therapy,severe hemorrhage like
APH,PPH,rupture uterus,cesarean section,first
trimester hemorrhage,thalassemiasand
sickling disorders in pregnancy
 ADVERSE REACTIONS
1. Tranfusion reaction
2. Infection
3. Volume overload
4. Others like hypothermia,citrate
toxicity,hyperkalemia,hypocalcemia and
rarely air embolism
 FIRST STAGE – COMFORTABLE POSITION
 ADEQUATE ANALGESIA
 Arrangement for oxygen,
 Digitalization maybe required in cardiac failur
e
due to severe anaemia
 Antibiotic prophylaxis
 SECONDSTAGE – CUT SHORTBYFORCEPS APPLICATION.
 Active managementof third stage
 During puerperium
 Adequate rest
 Iron and folate therapy for 3 months
 Infection if any should be treated energetically
 Careful watch for puerperal sepsis, failing lactation; sub
involution of uterus and thromboembolism
• There is derangement in red cell maturation with
the production in the bone marrow of abnormal
precursors known as megaloblasts due to
impaired DNA synthesis.
• Vit B12 or folate defieciency or both.
• Vit B12 deficiency is rare in pregnancy.
• In pregnancy, due to folic acid deficiency.
CAUSES
• Megaloblastic anaemia of pregnancy (temperate
climate)
• Nutritional megaloblastic anaemia
• Addisonian pernicious anaemia (rare)
• Megaloblastic anaemia of malabsorption
syndrome.
FOLIC ACID DEFICIENCY…
• Inadequate intake due to:
– Nausea, vomiting, loss of appetite.
– Dietary insufficiency – green leafy veg, cauliflower,
spinach, liver, kidney
• Increased demand:
– Increased maternal tissue including red cell
volume.
– Developing product of conception.
• Diminished absorption:
• Abnormal demand:
– Twins, infection, haemorrhagic states.
• Failure of utilisation:
– Anticonvulsant drugs.
• Diminshed storage:
– Hepatic disorders and vitamin c
deficiency.
• Iron deficiency anaemia:
INCIDENCE
• 0.5 – 3%
• Common in multiparae and multiple
pregnancy.
CLINICAL
FEATURES
O/E
HAEMATOLOGICAL EXAMINATION AND OTHER
BLOOD VALUES
• Hb – 10gm%
• Stained blood film: hypersegmentation of the
neutrophils, macrocytosis and anisocytosis.
Megaloblasts.
• MCV- 100 µm3
• MCH –high, MCHC –normal
• Associated leucopenia and
thrombocytopenia
• Serum iron is normal or high
• Serum folate – 3ng/ml
• Serum B12 level below <90 pg/ml
• Bone marrow – megaloblastic erythropoiesis
COMPLICATIONS
• Abortion
• Dysmaturity
• Prematurity
• Abruptio placentae
• Fetal malformation
PROPHYLACTIC
THERAPY
• All woman of reproductive age should be given
400µg of folic acid daily.
• Additional amount (4mg) should be given where
demand is high.
HAEMOGLOBINOPATHIES
SICKLE CELL ANAEMIA
• Hereditary disorders in which the red cells contain
Hb-S.
• Produced by substitution of valine for glutamic
acid at the position 6 of the β-chain of normal
haemoglobin.
PATHOPHYSIOLOGY
• Red cells with HbS in oxygenated state behave
normally but in the deoxygenated state it
aggregates, polymerises and distort the red cells
to sickle.
• These sickle shaped cells block the
microcirculation due to their rigid structure.
EFFECTS ON PREGNANCY
• Increased incidence of abortion,prematurity,
IUGR and fetal loss.
• Perinatal mortality is high.
• Preclampsia, postpartum haemorrahage and
infection is increased.
EFFECTS ON THE DISEASE.
• There is chance of sickle cell crisis which usually
occurs in the last trimester.
• Haemolytic crisis
• Painful crisis.
MANAGEMENT
• Preconceptional counselling
• During pregnancy: antenatal supervision, regular
blood transfusion at 6 weeks interval.
• Contraception: sterilisation, oral pill, barrier
method is ideal.
THALASSAEMIA SYNDROMES
• Commonly found genetic disorders of the blood.
• Basic defect is a reduced rate of globin chain
synthesis.
• As a result, the red cellsbeing formed with an
inadequate haemoglobin content.
• Types – alpha and beta (depending upon the
chain)
ALPHA THALASSAEMIA
• Incompatible with life.
• Α-peptide chain production is controlled by 4
genes, located on chromosome 16. Depending
upon the degree of deficient synthesis – 4 clinical
types.
• Mutation of one gene: no clinical or laboratory
abnormalities. Silent carrier
• Mutation in 2 – 4 genes: minor. Often goes
unrecognised and pregnancy is well tolerated.
• Mutation in 3 – 4 genes: Hb H disease. 
hemolytic anaemia.
• Mutation in all four genes: major. No alpha globin
chain. Fetus dies either in utero or soon after
birth.
BETA THALASSEMIA
• beta chain production is directed by 2 genes –
one on each copy of chromosome 11.
• Major – when mutation affect both the genes. –
red cell destruction- no erythropoiesis – blood
transfusion necessary for survival.
• Minor – mutation of one gene. – can tolerate
pregnancy –oral folic acid supplementation is
continued.
Anemia in Pregnancy is the most common medical condition

Anemia in Pregnancy is the most common medical condition

  • 1.
  • 2.
     What isAnaemia ? Anaemia is defined as reduction in circulating haemoglobin mass below the critical level.  The normal haemoglobin (Hb) is 12-14 gm%.  WHO has accepted up to 11 gm% as the normal haemoglobin level in pregnancy.  Therefore any haemoglobin level below 11gm in pregnancy should be considered as anaemia
  • 3.
     Anaemia inpregnancy is present in very high percentage of pregnant women in India.  Exact data is not available about the prevalence of nutritional anaemia. However according to WHO, the prevalence of Anaemia in pregnancy in south East Asia is around 56 %.  In India incidence of anaemia pregnancy has been noted as high as 40-80%.
  • 4.
    Total iron requirementis 1000 mg.  Fetus and placenta -- 300 mg  ↑ in red cell mass – 500 mg  Basal loss – 200 mg Average requirement is 4-6mg/day.  2.5 mg/day in early pregnancy  5.5 mg/day from 20-32 weeks  6-8 mg/day from 32 weeks onwards
  • 5.
     Anaemia isoften classified as Mild degree (9-11 gm %) Moderate (7-9 gms %) Severe (4-7 gm %) Very severe (<4gm %)  It is also classified according to Haematocrit (PCV) %.
  • 6.
    Antenatal Period -Poor weight gain -Pretermlabour -PIH -Placenta Previa -PROM Postnatal Period -Postnatal sepsis -Sub involution -Embolism Intranatal Period -Dysfunctional Labour -Intranatal -Hemorrhage -Shock -Cardiac Failure -Anaethesia risk MATERNAL COMPLICATIONS
  • 7.
    • • • • • Prematurity Low birth weight Poorapgar score Foetal distress Neonatal Anaemia FETAL AND NEONATAL COMPLICATIONS
  • 8.
     Physiological  Nutritional:Iron deficiency  Folate &/or Vit B12 deficiency Dimorphic  Hemorrhagic: Acute or Chronic  Hemoglobinopathies  Hemolytic: Congenital or acquired  Aplastic anaemia
  • 9.
    Symptoms  Fatigue  Lossof appetite  Digestive upset  Dyspnoea  Palpitation Signs Pallor Pale nails Koilonychias Pale Tongue Severe Case - Oedema
  • 10.
    • CBC • PheripheralSmear – Hypochromic Microcytosis Poikilocytosis Anisocytosis • MCV, MCH, MCHC • TIBC • Serum Iron • Serum Ferritin • Free erythrocyte protoporphyrin • Bone marrow examination • Urine examination • Stool examination • Serum protein
  • 11.
     Serum Folate RBC folate  Serum Vit B12  Serum Bilirubin  Coombs test  HB electrophoresis  NESTROF test  Red cell osmotic fragility
  • 12.
     Routine screeningfor anaemia for adolescent girls from school days  Encouraging iron rich foods  Fortification of widely consumed food with iron  Providing iron supplementation from school days  Annual screening for those with risk factors
  • 13.
     PROPHYLAXIS OFNON-PREGNANT WOMEN – 60 MG OF ELEMENTAL IRON DAILY FOR 3 MONTHS.  Iron supplementation during pregnancy.  Routine iron supplementationis debatable in western countries  It has to be given in non-industrialized countries  W.H.O RECOMMENDATION: Universal oral iron supplementation for pregnant women(60 mg of elemental iron and400 µg of folic acid) for 6 months in pregnancy and additional of 3 months post-partum where the prevalence is morethan 40%.
  • 14.
     MINISTRY OFHEALTH, GOVT. OF INDIA RECOMMENDATION: [CSSM] 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.  Treatment of hook worm infestation  Single albendazole (400 mg)or mebendazole (100 mg x BD x 3days)  Change in defecation habits and avoidance of walking b a r e footed.
  • 15.
    PULSES, CEREALS, JAGGERY,BEETROOT, GREEN LEAFY VEGETABLES,MEAT,LIVER,EGG,FISH,LEGUMES,DRY BEANS
  • 16.
     MOTHER  PREGNANCY- 1. Cardiacfailure at 30-34 wks of pregnancy 2. Increased susceptibility to infection 3. Preterm labour 4. Preeclampsia  LABOUR- 5. Uterine inertia 6. Post partum haemorrhage 7. Cardiac failure 8. shock
  • 17.
     Puerperium 1. Cardiacfailure 2. Puerperal sepsis 3. Subinvolution 4. Failing lactation 5. Chronic ill health,backache  FETUS&NEONATE 6. Prematurity 7. IUGR 8. Increased perinatal death 9. Decreased iron stores in neonate
  • 18.
     ORAL IRONTHERAPY 1. Safe,inexpensive and effective way to administer iron 2. National nutritional anemia prophylaxis program suggest 60 milligrams of elemental iron and 500 micrograms of folic acid daily 3. However it is suggested that 120 milligram of elemental iron and 1 milligram of folicacid are the optimum daily dose needed
  • 19.
    SALT TABLET ELEMENTAL IRON Ferroussulfate 200mg 60mg[30%] Ferrous fumarate 200mg 66mg[33%] Ferrous gluconate 320mg 36mg[12%] Ferrous succinate 100mg 35mg[35%] Ferric ammonium citrate 125mg 25mg[17-22%] Ferrous ascorbate ------ 100mg Carbonyl iron ------- 90mg Sodium feredetate ------- 231mg Hb preparation 2.1g [0.33%]
  • 20.
     SIDE EFFECTSOF ORAL IRON A. UPPER GI TRACT Nausea,gastric discomfort,loss of apetite,staining of teeth A. LOWER GI TRACT Constipation,diarrhoea,flatulance
  • 21.
     PARENTRAL IRONTHERAPY  Preparation Iron sucrose-Imax S[100mg/5ml],orofer s[50mg /2.5ml] Iron sorbital citric acid complex- jectocos Iron dextran-imferon
  • 22.
     Intramuscular iron 1.0.5ml test dose should be given 2. 75/100mg/day is given daily on alternate days 3. Given deep Im by Z-techniue to prevent skin staining 4. Side effects- painful,discolouration,injection abscess
  • 23.
     INTRAVENOUS IRON 1.Formula-0.66*% deficit of Hb*wt in kg=mg of iron 2. Total dose in mg/50=ml of imferon 3. Total dose is given in normal saline  COMPLICATION Local-thrombophlebitis at IV site Systemic-malaise,fever,arthralgia,utricaria lymphadenopathy
  • 24.
     BLOOD TRANFUSION 1.Indicated insevere anemia at any GA,moderate anemia beyond 36wks and when there is a failure of response to iron therapy,severe hemorrhage like APH,PPH,rupture uterus,cesarean section,first trimester hemorrhage,thalassemiasand sickling disorders in pregnancy
  • 25.
     ADVERSE REACTIONS 1.Tranfusion reaction 2. Infection 3. Volume overload 4. Others like hypothermia,citrate toxicity,hyperkalemia,hypocalcemia and rarely air embolism
  • 26.
     FIRST STAGE– COMFORTABLE POSITION  ADEQUATE ANALGESIA  Arrangement for oxygen,  Digitalization maybe required in cardiac failur e due to severe anaemia  Antibiotic prophylaxis
  • 27.
     SECONDSTAGE –CUT SHORTBYFORCEPS APPLICATION.  Active managementof third stage  During puerperium  Adequate rest  Iron and folate therapy for 3 months  Infection if any should be treated energetically  Careful watch for puerperal sepsis, failing lactation; sub involution of uterus and thromboembolism
  • 29.
    • There isderangement in red cell maturation with the production in the bone marrow of abnormal precursors known as megaloblasts due to impaired DNA synthesis.
  • 30.
    • Vit B12or folate defieciency or both. • Vit B12 deficiency is rare in pregnancy. • In pregnancy, due to folic acid deficiency.
  • 31.
    CAUSES • Megaloblastic anaemiaof pregnancy (temperate climate) • Nutritional megaloblastic anaemia • Addisonian pernicious anaemia (rare) • Megaloblastic anaemia of malabsorption syndrome.
  • 32.
    FOLIC ACID DEFICIENCY… •Inadequate intake due to: – Nausea, vomiting, loss of appetite. – Dietary insufficiency – green leafy veg, cauliflower, spinach, liver, kidney • Increased demand: – Increased maternal tissue including red cell volume. – Developing product of conception. • Diminished absorption: • Abnormal demand: – Twins, infection, haemorrhagic states. • Failure of utilisation: – Anticonvulsant drugs.
  • 33.
    • Diminshed storage: –Hepatic disorders and vitamin c deficiency. • Iron deficiency anaemia:
  • 34.
    INCIDENCE • 0.5 –3% • Common in multiparae and multiple pregnancy.
  • 35.
  • 36.
  • 37.
    HAEMATOLOGICAL EXAMINATION ANDOTHER BLOOD VALUES • Hb – 10gm% • Stained blood film: hypersegmentation of the neutrophils, macrocytosis and anisocytosis. Megaloblasts. • MCV- 100 µm3 • MCH –high, MCHC –normal • Associated leucopenia and thrombocytopenia • Serum iron is normal or high • Serum folate – 3ng/ml • Serum B12 level below <90 pg/ml • Bone marrow – megaloblastic erythropoiesis
  • 38.
    COMPLICATIONS • Abortion • Dysmaturity •Prematurity • Abruptio placentae • Fetal malformation
  • 39.
    PROPHYLACTIC THERAPY • All womanof reproductive age should be given 400µg of folic acid daily. • Additional amount (4mg) should be given where demand is high.
  • 40.
  • 41.
  • 42.
    • Hereditary disordersin which the red cells contain Hb-S. • Produced by substitution of valine for glutamic acid at the position 6 of the β-chain of normal haemoglobin.
  • 43.
    PATHOPHYSIOLOGY • Red cellswith HbS in oxygenated state behave normally but in the deoxygenated state it aggregates, polymerises and distort the red cells to sickle. • These sickle shaped cells block the microcirculation due to their rigid structure.
  • 44.
    EFFECTS ON PREGNANCY •Increased incidence of abortion,prematurity, IUGR and fetal loss. • Perinatal mortality is high. • Preclampsia, postpartum haemorrahage and infection is increased.
  • 45.
    EFFECTS ON THEDISEASE. • There is chance of sickle cell crisis which usually occurs in the last trimester. • Haemolytic crisis • Painful crisis.
  • 46.
    MANAGEMENT • Preconceptional counselling •During pregnancy: antenatal supervision, regular blood transfusion at 6 weeks interval. • Contraception: sterilisation, oral pill, barrier method is ideal.
  • 47.
    THALASSAEMIA SYNDROMES • Commonlyfound genetic disorders of the blood. • Basic defect is a reduced rate of globin chain synthesis. • As a result, the red cellsbeing formed with an inadequate haemoglobin content. • Types – alpha and beta (depending upon the chain)
  • 48.
    ALPHA THALASSAEMIA • Incompatiblewith life. • Α-peptide chain production is controlled by 4 genes, located on chromosome 16. Depending upon the degree of deficient synthesis – 4 clinical types. • Mutation of one gene: no clinical or laboratory abnormalities. Silent carrier
  • 49.
    • Mutation in2 – 4 genes: minor. Often goes unrecognised and pregnancy is well tolerated. • Mutation in 3 – 4 genes: Hb H disease.  hemolytic anaemia. • Mutation in all four genes: major. No alpha globin chain. Fetus dies either in utero or soon after birth.
  • 50.
    BETA THALASSEMIA • betachain production is directed by 2 genes – one on each copy of chromosome 11. • Major – when mutation affect both the genes. – red cell destruction- no erythropoiesis – blood transfusion necessary for survival. • Minor – mutation of one gene. – can tolerate pregnancy –oral folic acid supplementation is continued.