ANAEMIA IN PREGNANCY

BY

Dr. Shumaila Zia

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-- Sever anaemia------- Very sever anaemia- 7-8.9 gm /dl < 7gm /dl < 4gm/dl

ETIOLOGY

1 There are 3 main causes: Erythrocyte production: (hypo proliferative anemia )

. Fe deficiency 2 3 . Folic acid . Vitamin B12

RBC destruction: RBC loss:

90% anemia in pregnancy is due to Fe deficiency

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

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

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 - Giddiness - Breathlessness

EFFECTS OF ANAEMA IN PREGNANCY  .

Mother :

 High output Cardiac failure (more likely if precelampsia present. inadequate tissue oxygenation increase requirments for excessive blood flow )  PPH  Predisposes to infection  Risk of thrombo-embolism  Delayed general physical recovery esp after c. section 

Fetus:

. IUGR . Preterm birth . LBW . Depleted Fe store . Delayed Cognitive function.

INVESTIGATIONS

    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 :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.

 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.

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

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  In tolerance 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 theraphy in the form of I/M or I/V iron - I/M : ( Iron sorbitol) with “Z” technique - I/V : (iron sucrose)  Iron neede = (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 Dihydrofolicacid then Tetrahydro-folicacid . (THF) e 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.

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.

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 F/Hx. of neural tube defect - 4mg folic acid/day.

Vitamins B

12

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 B 12 Deficiency:

 Vit B 12 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%.

 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.

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 Thallassemia 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.

 Sever anaemia.

 Diagnosed in paediatric era.

 T/m: is blood transfusion.

ALPHA THALASSAEMIA:

 Both heterozygous & homozygous forms exist.

 Alpha thallassaemia trait.

 HbH disease.

 Alpha thallassaemia major.

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)

 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

SCD



Diagnosis

: - Hb. Electrophoresis - Sickledext test is screening test 

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

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