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Anaemia
Anaemia
Anaemia
Anaemia
Anaemia
Anaemia
Anaemia
Anaemia
Anaemia
Anaemia
Anaemia
Anaemia
Anaemia
Anaemia
Anaemia
Anaemia
Anaemia
Anaemia
Anaemia
Anaemia
Anaemia
Anaemia
Anaemia
Anaemia
Anaemia
Anaemia
Anaemia
Anaemia
Anaemia
Anaemia
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Anaemia
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Anaemia
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Anaemia

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  • 1. Dr.Suresh Babu Chaduvula Professor Dept. of OBGYN College of Medicine King Khalid University Abha, KSA
  • 2.  Commonest medical disorder.  High incidence in underdeveloped countries Importance:  Increased Maternal morbidity & mortality  Increased perinatal mortality
  • 3. Definition: By WHO Hb. < 11 gm /dl (or Hematocrit <32%). Mild anaemia -------- 9 -10.9 gm /dl Moderate anaemia--- 7-8.9 gm /dl Sever anaemia-------- < 7gm /dl Very sever anaemia-- < 4gm/dl
  • 4. 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. • 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
  • 6. 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
  • 7.  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
  • 8. 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
  • 9.  . 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 cesarean section  Fetus: .IUGR . Preterm birth . LBW . Depleted Fe store . Delayed Cognitive function.
  • 10.  Hb  Haematocrit or PCV  RBC Indices: - Low MCV - Low MCH - Low MCHC  Peripheral blood picture : Microcytic Hypochromic anemia .
  • 11.  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
  • 12.  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.  Ankylostoma duodenale – a hook worm that will suck blood from small intestine.
  • 13.  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
  • 14.  Choice of method: It depends on three main factors:  Severity of the anemia  Gestational Age.  Presence of additional risk factor
  • 15.  Recommended supplementation for non-anaemiac 30 - 60mg /day of elemental iron  Anemic gravidas 120 –240mg / per day  Intolerance 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.  Moderate anaemia: 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 needs = (Normal Hb – Pt. Hb) X Wt in Kg X 2.21+1000)
  • 17. 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 expected in 7-14 d Blood transfusion:  may be required to treat severe anemia near term or when some other complication such as placenta previa present.  Gross anemia  Packed red cells transfusion (under cover of loop diuretic)  Exchange transfusion (under cover of loop diuretic)
  • 18. Side effect of Fe Oral therapy: . G. I upset. . Constipation. . Diarrhoea. Parentral: - skin discolouration - local abscess - allergic reaction - Fe over load.
  • 19.  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
  • 20. At cellular level Folic acid reduced to Dihydrofolicacid then to Tetrahydro-folicacid (THF) is required for cell growth & division. So more active tissue reproduction & growth - more dependent on supply of folic acid. So bone marrow and epithelial lining are therefore at particular risk.
  • 21. 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.
  • 22. Diagnosis: Increased MCV ( > 100 fl) Peripheral smear: - Macrocytosis, hypochromia - Hypersegmented neutrophils (> 5 lobes) - Neutropenia - Thrombocytopenia Low Serum folate level. Low RBC folate.
  • 23.  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 Family history of neural tube defect - 4mg folic acid/day.
  • 24.  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.  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.
  • 26. 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.  The synthesis of globin chain is partially or completely suppressed resulting in reduced Hb. content in red cells with shortened life span.  TYPES: - Alpha thalassemia. - Beta thalassemia: . Major . minor
  • 28.  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.  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.  Homozygous inheritance from both parents.  Sever anaemia.  Diagnosed in paediatric era.  T/m: is blood transfusion. .
  • 31. ALPHA THALASSAEMIA:  Both heterozygous & homozygous forms exist.  Alpha thallassaemia trait.  HbH disease.  Alpha thallassaemia major
  • 32.  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.
  • 33.  Sickeling crises frequently occurs in pregnancy, puerperium and in state of hypoxia.  Increased incidence 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
  • 34.  Diagnosis: - Hb. Electrophoresis - Sickling 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 contraindicated), blood transfusion
  • 35.  Comfortable Position  Adequate analgesia  O2 inhalation  Low threshold of assisted delivery Prophylactic Ergometrine  Prophylactic antibiotics  Continue iron &folate therapy for 3 months after delivery  Appropriate contraceptive advice
  • 36. Thank You All

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