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ANAEMIA IN PREGNANCY
BY
Dr. Shumaila Zia
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ANAEMIA IN PREGNANCY
Commonest medical disorder. High incidence in underdeveloped countries Increased Maternal morbidity & mortality Increased perinatal mortality
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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
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ETIOLOGY
There are 3 main causes:
1- Erythrocyte production: (hypo proliferative anemia )
. Fe deficiency
. Folic acid
. Vitamin B12
2- RBC destruction:
3- RBC loss:
90% anemia in pregnancy is due to Fe deficiency
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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 MCH2-3 fold increase in Fe requierment.10-20 Fold increase in folate requirement
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Common Anaemias in pregnancyCommon 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
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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 -------1360mg350mg subtracted (saved as a result of
amennorrhoea)So actual extra demand ----------------------1000mgFull iron stores --------------------------------1000mg
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ETIOLOGY OF IRON DEFICIENCY ANAEMIA Depleted iron stores – dietary lack, chronic renal failure,
worm infestation, chronic menorrhagiaChronic 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
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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.
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INVESTIGATIONS
Hb Haematocrit RBC Indices: - Low MCV
- Low MCH - Low MCHC - Low PCV Peripheral blood picture : Microcytic Hypochromic anaemia .
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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
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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.
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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 anaemiaGestational Age.Presence of additional risk factor
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MANAGEMENTRecommended supplementation for non-anaemiac
30 - 60mg /day of elemental ironAnaemic gravidas 120 –240mg / per dayIn tolerance to iron tablets – enteric coated tablet /
liquid suspensionSupplementation 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
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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)
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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)
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MANAGEMENT
Side effect of Fe Oral therapy:
. G. I upset.
. Constipation.
. Diarrhoea.
Parentral:
- skin discolouration
- local abscess
- allergic reaction
- Fe over load.
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MEGALOBLASTIC ANAEMIAComplicates upto 1% of pregnanciesCharacterized 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
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FOLATE DEFICIENCY ANAEMIAAt 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.
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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.
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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.
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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.
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Vitamins B12 DeficiencyIt is rare
Occurs in patients with gastrectomy , ileitis, illeal resection, pernicious anaemia, intestinal parasites.
Diagnosis:Peripheral smearVitamin B12 level < 80 pico g/ml
Treatment of B12 Deficiency: Vit B12 1mg I/M weekly for 6 weeks.
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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.
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HAEMOGLOBINOPATHIESDEFINITION: 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)
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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
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Beta thallassemia minor
Beta Thallassemia traitHeterozygous 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.
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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.
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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.
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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.
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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
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SCD
Diagnosis:
- Hb. Electrophoresis
- Sickledext test is screening testManagement:
- 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
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Management During labour
Comfortable PositionAdequate analgesiaO2 inhalationLow threshold of assisted deliveryAvoid ergometrineProphylactic antibioticsContinue iron &folate therapy for 3 mo after
deliveryAppropriate contraceptive advice