2 ANAEMIA IN PREGNANCY Commonest medical disorder. High incidence in underdeveloped countriesIncreased Maternal morbidity & mortalityIncreased perinatal mortality
3 ANAEMIA IN PREGNANCYDefinition: By WHO Hb. < 11 gm /dl (or haematocrit <32%). Mild anaemia gm /dl Moderate anaemia gm /dl Sever anaemia < 7gm /dl Very sever anaemia-- < 4gm/dl
4 ETIOLOGYThere 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
5 Physiological changes in pregnancy Plasama volume % (by 34weeks)But RBC mass only 25%Results in haemodilution :HbHaematocritRBC countNo change in MCV or MCH2-3 fold increase in Fe requierment.10-20 Fold increase in folate requirement
7 Common Anaemias in pregnancy Common types:Nutritional deficiency anaemias- Iron deficiency- Folate deficiency- Vit. B12 deficiencyHaemoglobinopathies:- Thallassemias- SCDRare types:- Aplastic- Autoimmune hemolytic- Leukemia- Hodgkin’s disease- Paroxysmal nocturnal haemoglobinurea
8 IRON DEFICIENCY ANAEMIA Iron required for fetus and placenta mg.Iron required for red cell increment mgPost partum loss mg.Lactation for 6 months - 180mg.Total requirement mg350mg subtracted (saved as a result of amennorrhoea)So actual extra demand mgFull iron stores mg
9 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 FEATURESSymptoms usually in severe anaemia- Fatigue- Giddiness- Breathlessness
10 EFFECTS OF ANAEMA IN PREGNANCY Mother :High output Cardiac failure (more likely if precelampsia present. inadequate tissue oxygenation increase requirments for excessive blood flow )PPHPredisposes to infectionRisk of thrombo-embolismDelayed general physical recovery esp after c. sectionFetus: . IUGR. Preterm birth. LBW. Depleted Fe store. Delayed Cognitive function.
12 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.
13 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.
14 MANAGEMENT Objectives: 1- To achieve a normal Hb by end of pregnancy 2- To replenish iron storesTwo ways to correct anaemia:I- Iron supplementation Oral Fe. Parenteral FeII- Blood transfurionChoice of method:It depends on three main factors:Severity of the anaemiaGestational Age.Presence of additional risk factor
15 MANAGEMENTRecommended supplementation for non-anaemiac mg /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
16 MANAGEMENTSevere 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* )
17 MANAGEMENTDose 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 hoursMarked increase in reticulocyte count expecred in 7-14 dBlood transfusion:may be required to treat severe anaemia near term or when some other complication such as placenta praevia present.Gross anaemiaPacked red cells transfusion (Under cover of loop diuretic)Exchange transfusion (Under cover of loop diuretic)
18 MANAGEMENTSide effect of Fe Oral therapy: . G. I upset. . Constipation. . Diarrhoea. Parentral: - skin discolouration - local abscess - allergic reaction - Fe over load.
19 MEGALOBLASTIC ANAEMIA Complicates 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 exposureto sulfa drugs or hydroxyurea- Vitamin B12 deficiency
20 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.
21 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.
23 FOLATE DEFICIENCY ANAEMIA Daily folate requirement for :Non pregnant women microgramPregnant woman – microgramUsually folic acid present in diets like fresh fruits and vegetables and destroyed by cooking.Folate deficiency:mg folic acid/dayIf F/Hx. of neural tube defect- 4mg folic acid/day.
24 Vitamins B12 Deficiency It is rare Occurs in patients with gastrectomy , ileitis, illeal resection, pernicious anaemia, intestinal parasites.Diagnosis:Peripheral smearVitamin B12 level < 80 pico g/mlTreatment of B12 Deficiency:Vit B12 1mg I/M weekly for 6 weeks.
25 HAEMOGLOBINOPATHIES. Normal adult Hb. after age of 6 month, HbA---97%, HbA2---( %), 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.
26 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)
27 THALASSAEMIASThe 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
28 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.
29 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.
30 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.
31 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.
32 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 birthgrowth restriction, premature birth and intrapartum fetal distress with increased perinatal mortality.Sickle cell trait:(carrier state)Does not pose any significance clinical problems
33 SCD Diagnosis: - Hb. Electrophoresis - Sickledext test is screening testManagement:- No curative Tx.- only symptomatic- Well hydration, effective analgesia, prophylacticantibiotics, O2 inhalation, folic acid, oral ironsupplement (I/V iron is C/I), blood transfusion
35 Management During labour Comfortable PositionAdequate analgesiaO2 inhalationLow threshold of assisted deliveryAvoid ergometrineProphylactic antibioticsContinue iron &folate therapy for 3 mo after deliveryAppropriate contraceptive advice
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