ANEMIA IN PREGNANCY

Dr Virupaksha Ajjammanvar
• Megaloblastic anemia
• Hemoglobinopathies
• Dimorphic anemia
 Megaloblastic anemia
• In megaloblastic anemia,there is derangement in red
cell maturation with production in the bone marrow of
abnormal precursors known as megaloblasts due to
impaired DNA synthesis.

• Causes
Folic acid deficiency
Vitamin B12 deficiency
 Folic acid deficiency
• Megaloblastic anemia in pregnancy is almost always
due to folic acid deficiency.
• Folic acid is a water soluble vitamin stored in liver.
• Normal folate store is sufficient for 6 weeks.After 3
weeks of a deficient folate diet, the serum level
falls.Two weeks later there is hypersegmentation of
neutrophilis and after 17week RBC folate levels drop.
• Daily folate requirement during pregnacy is 200mcg
• Folate deficiency rarely occurs in the fetus and it is
not associated with any significant perinatal
mortality.
Causes of folic acid deficiency in pregnancy

• Inadequate intake due to:

1) Nausea,vomiting and loss of appetite
2)Dietary insufficiency –the main sources of folic acid
are green leafy vegetables, cauliflower, spinach,
liver, kidney.
Excessive cooking destroys much of folate in food
 Causes of folic acid deficiency in pregnancy

• Increases demand due to:

1)Increased maternal tissue including red cell
volume
2)growing fetus
3)multiple pregnancy
• Diminished absorption: Intestinal malabsorption
syndrome
Causes of folic acid deficiency in pregnancy

• Abnormal demand:
1)Infection
2)Hemorrhage due to peptic ulcer, hookworm
infestation, hemorrhoids, hemolysis due to chronic
malaria, sickle cell anemia, or hemoglobinopathy.
• Failure of utilisation:Anticonvulsants drugs,infection
• Diminished storage
• Iron defieciency anemia
 Vitamin B12 deficiency

• Vitamin B12 deficiency is rare in pregnancy

• Daily requirement in nonpregnant 2mg and during
pregnancy 3mg.
• Vitamin B12 is first bound to intrinsic factor
secreated by gastric parietal cells and absorbed in
distal ileum.
• Strict vegetarians may need supplemenatation.
 Causes of Vitamin B12 deficiency
• Strict vegetarian diet
• Gastritis
• Gastrectomy
• Bariatric surgery
• Ileal bypass
• Crohns disease
• Drugs-COCs,metformin,proton pump inhibitors
• Addisonian pernicious anemia
• Malabsorption syndrome
 Incidence

• 0.5 to 3%
• It is more common in multiparae and multiple
pregnancy.
• An elevated homocysteine level is found when serum
folate levels are low.
• High homocyteine level are at increased risk of
preeclampsia,preterm labour and IUGR
• In folate def :Normal methylmalnote
• In Vit B12 def:Increased methylmalnote
 Clinical features

• Onset is insidious and first revealed in last trimester

or may be acutely manifested in early puerperium
• Anorexia or protracted vomiting
• Occasional diarrhoea
• Constitutional symptoms like unexplained fever
 On examination

• Pallor of varying degree

• Ulceration of mouth(glossitis) and tongue
• Hemorrhagic patches under the skin and conjunctiva
• Enlarged liver and spleen
• Features of preeclampsia ( two and half times
increased)
 Investigation
• Hemoglobin level is below 10gm%
• Peripheral smear: a)Hypersegmentation of
neutrophilis b)macrocytosis and anisocytosis
c)giant polymorphs d)megaloblasts e)Howel jolly
bodies
• MVC and MCH increases but MCHC will be normal.
• Associated leukopenia and thrombocytopenia
 Investigation-cont
• Serum iron is normal or high and total iron binding
capacity is low
• Red cell folate is below 3ng/ml
• Serum vitamin B12 level is below 90pg/ml
• Serum bilirubin may be raised
• Bone marrow megaloblastic erthropoiesis
Complication of Megaloblastic anemia
• Miscarriage
• Dymaturity
• Prematurity
• Abruptio placentae
• Fetal malformation(cleftlip,cleft palate,neural tube
defects)
 Prophylactic therapy

• All women of reproductive age should be given

400mcg of folic acid daily.
• Additional 4mg where demand is high.
 Specific therapy
• Folic acid 4mg orally continued for at least 4weeks
following delivery.
• Supplementation of 1mg of folic acid daily along with
iron and nutritious diet can improve pregnancy
induced megaloblastic anemia by 7-10days.
• Response is evidenced by 1)sense of well being and
increased appetite 2)increase in
reticulocyte,leukocyte and thrombocyte count
3)rise in hemoglobin level
 Specific therapy -cont
• Folic acid should never be given without
supplemental iron
• IM Vit b12 100mg daily or alternate days when
response to folic acid alone is not adequate.
• Ascorbic acid 100mg tablet thrice daily enchances
the action of folic acid by converting it into folinic
acid
 Hemoglobinopathies
• Sickle cell hemoglobinopathies are herediatory
disorders. It is caused by a point mutation in the
beta globin gene on chromosome 2
• Gene mutation-when homozygous the individual
has sickle cell anemia(Hb-SS).She has small
quantity of fetal Hb but no HbA. Heterozygous
individual has sickle trait(HbAS).55-60% HbA and
35-40% of HbS.
• Sickle cells life span 5-10days.
 Prevalance

• Highest in Africa and ranges from 20-50%

 Sickle cell trait
• Hb-S comprises 30-40% of total Hb,rest being Hb-
A1,Hb-A2, and Hb-F.
• If the husband is carrier, 25% chance that infant will
be homozygous sickle cell disease and 50% sickle
trait.
• Preconceptional counseling should be done to know
whether the husband carries the trait or not.
• The patient requires iron supplementation.Hb-S
concentration is low, sickle cell crisis is rare.
• Hematuria and urinary infection are quite common
 Sickle cell disease

• Hb-SS is transmitted equally by males and females.

• Partner must be tested
• Temination of pregnancy if major hemoglobinopathy
diagnosed on prenatal diagnosis
 Pathophysiology

• Red cells with HbS in oxygenated state behave

normally but in deoxygenated state it
aggregates,polymerizes and distort the red cells into
sickle.
• Sickling phenomenon is precipitated by
infection,acidosis,dehydration,hypoxia, and cooling.
• Increased destruction leads to hemolysis,anemia and
jaundice.
 Diagnosis
• Refractory hypochromic anemia
• Sickling test
• Persistent reticulocytosis(10-20%)
• High serum iron level
• Electrophoresis
 Effect on pregnancy
• Miscarriage(25%)
• Prematurity
• Preeclampsia
• PPH
• Infection
• Maternal morbidity due to infection,cerebrovascular
accident and sickle cell crisis
• Maternal death increased upto 25% due to
pulmonary infarction,acute chest syndrome,CCH and
embollism
 Effect on pregnancy-continued
• IUGR
• Fetal loss
 Effects on disease
Sickle cell crisis usually occurs in last trimester
Two types 1) Hemolytic crisis
2) Painful crisis

• Hemolytic crisis: Due to hemolysis with rapidly

developing anemia along with jaundice . Associated
leukocytosis and fever.
• Painful(vaso-occlusive) :Vascular occlusion of the
various organs by capillary thrombosis results in
infarction
 Management

Preconceptional counceling:Prenatal identification of

homozygous state of the disorder is an indication for
early termination of pregnancy.
 Management-During pregnancy

• Careful antenatal supervision

• Air traveling in unpressurized aircraft is to be avoided
• Prophylactic folic acid 1mg tablet daily
• Iron supplementation only in cases of iron deficiency
 Management-During pregnancy

• Prophylactic booster or exchange blood transfusion.

Objective of transfusion to keep hematocrit value
>25%,HbA >20%and concentration HbS under 50 %
• Infection or unusal symptoms requires
hospitalization. Pencillin prophylaxis is given to all
patients with SCD
• Hydroxy urea is used as a disease modifying drug.
 Management-Labor and delivery
• Vaginal delivery is preferred.
• The labor is to conducted like in anemia
• Continuous oxygen therapy to maintain PaO2>94%
• Anoxia is to avoided during anaesthesia. Epidural
anesthesia preferred
• Adequate fluid infusion to avoid dehydration and
acidosis
 Management-Labor and delivery

• Cesarean section only for obstetric indication

• Routine antibiotic in puerperpium to prevent
infection
• Thromboprophylaxis (LMWH) should be given during
pregnancy and puerperium
• Cord blood sent for hemoglobinopathy
 Contraception

• Sterilisation
• Oral pill is contraindicated
• IUD is avoided
• Barrier method is safe and effective
 Thalassemia syndromes

• Commonly found genetic disorder, basic defect is

reduced rate of globin chain synthesis.
• Two types-Alpha thalassemia
Beta thalassemia
 Alpha thalassemia
Four clinical types depending upon degree of deficient
alpha peptide chain synthesis
1) Mutation of one gene-there is no clinical or
laboratory abnormalities. Subject remains as a silent
carrier.
2)Mutation of 2 gene-alpha thalessemia minor.
Pregnancy is well tolerated
3)Mutation of 3 genes-Hb H disease. These women suffer
from hemolytic anemia, during pregnancy anemia
deteriorates further.
4)Mutations of all 4 genes-Alpha thalassemia major.
 Alpha thalassemia
• Prenatal diagnosis: Alpha thaalessmia diagnosed by
CVS or aminocentesis
 Beta thalassemia

Beta chain production is directed by 2genes,one on

each copy chromosome 11
Beta thalassemia Major:Mutation affects both genes.
Beta thalassemia minor:Mutation one gene.B chain
production reduced by half.
Can be detected by CVS or amniocentesis
 Hematological findings

• Low MCV and MCH but normal MCHC

• Serum iron and total iron binding capacity are normal
or elevated
• Hb electrophoresis shows raised concentration hbA2
to more than 3.5% with normal or raised Hb F
• Serum bilirubin: 2-3mg%
• Anemia is mild
 Treatment

Thalassemia Major:
• Oral and IV iron therapy is contraindicated
• Requires careful monitoring, organs are affected due iron
overload.
• Patients requires repeated blood transfusions during pregnancy
• Oral folic acid supplementation is continued
• Frequent evaluation of fetal well being.
.
 Treatment-cont
• Majority of the women tolerate pregnancy well with
good maternal and fetal outcome.
• Thalassemia major patients are often small in
stature, with small pelvis.Cesarean delivery is needed
• Oral iron therapy in thalassemia minor is given when
lab diagnosis of iron deficiency is established
• Blood tranfusion rarely indicated
Thank you