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Presentation on theme: "ANAEMIA IN PREGNANCY BY Dr. Shumaila Zia."— Presentation transcript:


2 ANAEMIA IN PREGNANCY Commonest medical disorder.
High incidence in underdeveloped countries Increased Maternal morbidity & mortality Increased perinatal mortality

3 ANAEMIA IN PREGNANCY Definition: 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 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

5 Physiological changes in pregnancy
Plasama volume % (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


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

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

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.

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

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 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 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

15 MANAGEMENT Recommended supplementation for non-anaemiac mg /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

16 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* )

17 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)

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

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

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.

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.

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

Daily folate requirement for : Non pregnant women microgram Pregnant woman – microgram Usually folic acid present in diets like fresh fruits and vegetables and destroyed by cooking. Folate deficiency: mg folic acid/day If 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 smear Vitamin B12 level < 80 pico g/ml Treatment 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 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

28 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.

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 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

33 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


35 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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