Dr. Shumaila Zia


Commonest medical disorder.  High incidence in underdeveloped countries  Increased Maternal morbidity & mortality  Increased perinatal mortality

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

Vitamin B12 2RBC destruction: 3RBC loss: 90% anemia in pregnancy is due to Fe deficiency . Fe deficiency .Erythrocyte production: (hypo proliferative anemia ) . Folic acid .ETIOLOGY There are 3 main causes: 1.

 10-20 Fold increase in folate requirement .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.


Aplastic .SCD Rare types: .Autoimmune hemolytic .Vit. B12 deficiency  Haemoglobinopathies: .Hodgkin’s disease .Folate deficiency .Leukemia .Thallassemias .Iron deficiency .Common Anaemias in pregnancy Common types:  Nutritional deficiency anaemias .Paroxysmal nocturnal haemoglobinurea .

IRON DEFICIENCY ANAEMIA  Iron required for fetus and placenta ------.180mg.  Total requirement -------1360mg  350mg subtracted (saved as a result of amennorrhoea)  So actual extra demand ----------------------1000mg  Full iron stores --------------------------------1000mg .180mg.  Lactation for 6 months .500mg.  Iron required for red cell increment ------.500mg  Post partum loss --------.

chronic renal failure. CLINICAL FEATURES Symptoms usually in severe anaemia .Breathlessness .blood loss at time of delivery . worm infestation. chronic menorrhagia Chronic infections: ( like malaria) Repeated pregnancies : .with interval < 1 year .ETIOLOGY OF IRON DEFICIENCY ANAEMIA Depleted iron stores – dietary lack.multiple pregnancy.Giddiness .Fatigue .

LBW . IUGR . section      Fetus: .  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. . Depleted Fe store . Delayed Cognitive function.EFFECTS OF ANAEMA IN PREGNANCY  . Preterm birth .

Low MCH .Low PCV  Peripheral blood picture : Microcytic Hypochromic anaemia . .INVESTIGATIONS    Hb Haematocrit RBC Indices: .Low MCV .Low MCHC .

S.when serum iron level fall . ferritin :In healthy adults ferritin circulate in plasma in range of 15_300 pg/l.INVESTIGATIONS   Serum iron decreased (<12 micro mol / l) Total iron binding capacity :TIBC in non-pregnant state is 33% saturated with iron . in iron deficiency anemia it is the first test to become abnormal.<15% ofTIBC fall in saturation.the TIBC INCREASED.  .

Increased in iron def. . anemia. Serum transferrin receptor(TfR) : present on all cells as transmembrane protien that binds transferrin iron and transfer it to cell interior.  Bone marrow examination.  RFTS/LFTS.  Stool examination for ova .  Urine for haemturia.cyst and occult blood.

Parenteral Fe II.To achieve a normal Hb by end of pregnancy 2.  Presence of additional risk factor .Blood transfurion  Choice of method: It depends on three main factors:  Severity of the anaemia  Gestational Age. Oral Fe .Iron supplementation .MANAGEMENT  Objectives: 1.To replenish iron stores  Two ways to correct anaemia: I.

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.MANAGEMENT  Recommended supplementation for non-anaemiac 30 .  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).21+1000) .I/M : ( Iron sorbitol) with “Z” technique .preferably parenteral theraphy in the form of I/M or I/V iron .I/V : (iron sucrose)  Iron neede = (Normal Hb – Pt. Hb)* Wt in Kg*2.

 Gross anaemia  Packed red cells transfusion (Under cover of loop diuretic)  Exchange transfusion (Under cover of loop diuretic) .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.

Fe over load. G. . Diarrhoea. .local abscess .allergic reaction . .skin discolouration . Parentral: . I upset. Constipation.MANAGEMENT Side effect of Fe Oral therapy: .

MEGALOBLASTIC ANAEMIA   Complicates upto 1% of pregnancies Characterized by : .RBC with high MCV .Vitamin B12 deficiency  .Folate deficiency may occur after exposure to sulfa drugs or hydroxyurea . Usually caused by : .White blood cells with altered morphology (hypersegmented neutrophils).

FOLATE DEFICIENCY ANAEMIA At cellular level Folic acid reduced to Dihydrofolicacid then Tetrahydro-folicacid . So more active tissue reproduction & growth more dependant on supply of folic acid. (THF) e is required for cell growth & division. So bone marrow and epithelial lining are therefore at particular risk. .

. Woman taking anticonvulsants. . Hemolytic anemia. Multiple pregnancy.spherocytosis Maternal risk: Megaloblastic anemia Fetal risk: Pre-conception deficiency cause neural tube defect and cleft palate etc. . thalasemia H.FOLATE DEFICIENCY ANAEMIA Folic acid deficiency more likely if .

Low RBC folate.Neutropenia .Macrocytosis. . hypochromia .Thrombocytopenia Low Serum folate level.FOLATE DEFICIENCY ANAEMIA Diagnosis: Increased MCV ( > 100 fl) Peripheral smear: .Hypersegmented neutrophils (> 5 lobes) .

.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: .0mg folic acid/day If F/Hx. of neural tube defect .5-1.4mg folic acid/day.0.FOLATE DEFICIENCY ANAEMIA  Daily folate requirement for :  Non pregnant women -.

illeal resection. intestinal parasites. pernicious anaemia.Vitamins B12 Deficiency  It is rare Occurs in patients with gastrectomy .  Diagnosis:  Peripheral smear  Vitamin B12 level < 80 pico g/ml  Treatment of B12 Deficiency:  Vit B12 1mg I/M weekly for 6 weeks. . ileitis.

synthesis is controlled by genes.5-3.  HbA---97%.A2= 2alpha+2 delta globin chains. after age of 6 month.  4 Globin chains associated with haem complex. HbA2---(1.  Alpha chains by 4 gene.2 from each parent.  Hb.  Hb. .  Beta chains by 2 genes . A = 2 alpha +2 beta globin chains. HbF2--<1%.  Hb.  Normal adult Hb.F = 2 alpha+ 2 gamma globin chains.5%).HAEMOGLOBINOPATHIES.1 from each parent.  Hb.

abnormalities may be: . .Hetrozygous = inherited from one parent.Structure of globin chains-sickle cell disease.HAEMOGLOBINOPATHIES DEFINITION:  Inherited disorders of haemoglobin.Globin chain synthesis------thallassemia. (Sufferer of disease) .Homozygous = inherited from both parents.  Hb. (Carrier/trait of disease) .  Defect may be in: .

which then have shortened life span.Alpha thalassaemia. content in red cells. Major .THALASSAEMIAS  The synthesis of globin chain is partially or completely suppressed resulting in reduced Hb. minor .Beta thalassaemia: .  TYPES: . .

 Red cell indices: low MCV.  Partial suppression of the Hb. low MCH. Electrophoresis. synthesis.  Diagnostic test: Hb. Investigations: Hb----around 10 g/dl. . normal MCHC.Beta thallassemia minor  Beta Thallassemia trait  Heterozygous inheritance from one parent.  Most frequent encountered variety.  Mild anaemia.

. Testing.  Parenteral iron should be avoided.  If not responded ---I/M folic acid. because of iron overload.  Iron & folate supplements in usual dose.  Frequent Hb.  blood transfusion close to time of delivery.Beta Thallassemia Minor  Management:  Same as normal woman in pregnancy.

 Diagnosed in paediatric era. ALPHA THALASSAEMIA:  Both heterozygous & homozygous forms exist.  Alpha thallassaemia trait.  HbH disease.  T/m: is blood transfusion. .Beta Thallassaemia Major  Homozygous inheritance from both parents.  Sever anaemia.  Alpha thallassaemia major.

SICKLE CELL SYNDROME. when oxygen supply is reduced.  Structural abnormality.  Hb precipitates & makes the RBCs rigid & sickle shaped.  HbS . .susceptible to hypoxia.  Heterozygous----HbAS.  Autosomally inherited .  Homozygous-----HbSS.  Compound heterozygous---HbSC etc.

 Increased incidance of abortion and still birth growth restriction.  Sickle cell trait:(carrier state) Does not pose any significance clinical problems .Sickle Cell Disease (SCD)  Sickeling crises frequently occurs in pregnancy. puerperium &in state of hypoxia like G/A and Hag. premature birth and intrapartum fetal distress with increased perinatal mortality.

No curative Tx. oral iron supplement (I/V iron is C/I).SCD  Diagnosis: . prophylactic antibiotics. . Electrophoresis . O2 inhalation. effective analgesia.Hb. folic acid. blood transfusion .Well hydration.only symptomatic .Sickledext test is screening test  Management: .


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 .

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