Anaemia in pregnancy

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  • 1. Anaemia in Pregnancy
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  • 2. Normal Blood Standards
    Red blood corpuscles (RBCs):
    Number:
    > In females: 4.5-5 millions/mm3.
    Haemoglobin (Hb%):
    > In females: 12-14 gm/100 cc (dl) blood. During pregnancy: 10-12 gm/dl i.e. physiological anaemia due to the increase in plasma volume more than RBCs volume.
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  • 3. Normal Blood Standards
    Red blood corpuscles (RBCs):
    Haematocrit value:
    > It is the volume of packed RBCs in 100 cc of blood.
    > In females: 42%.
    Reticulocytes:
    > 0-2%. They are cells with remnants of the nucleus. Reticulocytosis indicates over active bone marrow as in haemolyticanaemia
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  • 4. Normal Blood Standards
    Leucocytes:
    A. Total leucocytic count:
    > 4.000-10.000/mm3. It increases during pregnancy to 9.500-10.500/mm3 and up to 16.000/mm3 during labour and the first week of puerperium.
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  • 5. Normal Blood Standards
    Leucocytes:
    B.Differentialleucocytic count:
    > Basophils 0-1%.
    > Eosinophils 3-5%.
    > Monocytes 3-8%.
    > Lymphocytes 20-30%.
    > Neutrophils 60-70%.
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  • 6. Normal Blood Standards
    Platelets:200.000-400.000/mm3.
    Bleeding time:2-4 minutes.
    Coagulation time:4-8 minutes.
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  • 7. Anaemia
    Definition:
    Anaemia is a reduction in the number of RBCs and haemoglobin content with a corresponding reduction in the oxygen carrying capacity of the blood.
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  • 8. 1.Iron Deficiency Anaemia
    2.Megaloblastic Anaemia:
    Folic Acid Deficiency Anaemia
    Vit. B12 Deficiency Anaemia (Addisonian Pernicious Anaemia)
    3.Haemolytic Anaemias
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  • 9. Iron Deficiency Anaemia
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  • 10. Iron Deficiency Anaemia
    Iron Deficiency Anaemia
    It is the most common type of anaemias (95%).
    Daily Requirements:Normal iron requirement is 10 mg/day of which 1mg is absorbed. Requirement increases during pregnancy to 15mg/ day.
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  • 11. Iron Deficiency Anaemia>Aetiology
    Inadequate intake of iron.
    Defective absorption of iron e.g. achlorhydria.
    Increased demand e.g. menstruation and pregnancy.
    Chronic blood loss e.g. abnormal uterine bleeding and piles.
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  • 12. Iron Deficiency Anaemia
    Clinical Picture:
    Symptoms:
    general symptoms of anaemia as:
    >easy fatigability,
    >headache,
    >dyspnoea,
    >palpitation.
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  • 13. Iron Deficiency Anaemia
    Clinical Picture:
    Signs:
    >Pallor which can be detected in the face, palm of the hand, nail bed and mucus membranes of the mouth and conjunctiva.
    > Angular stomatitis and red glazed tongue.
    > Nails are brittle, striated with loss of their lustre. Spooning of the nails may occur in severe cases.
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  • 14. Investigations
    RBCs, haemoglobin and haematocrit: below normal.
    Serum iron concentration: below normal (n=125 m g/dl).
    Iron binding capacity: below normal (n=400 m g/dl).
    Transferrin saturation: below normal (n= 30%).
    Blood film: microcytichypochromicanaemia.
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  • 15. Treatment
    Diet: liver, meat, kidney, eggs and green vegetables are rich in iron
    Oral iron therapy: ferrous sulphate or ferrous gluconate 300 mg t.d.s. after meals. Side effects: nausea, vomiting and constipation.
    Parenteral iron therapy: Preparations:
    >Iron-dextran complex: IV or IM injection.
    > Iron-sorbitol-citrate complex: IM injection only.
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  • 16. Treatment
    Side effects:
    IM injection is irritant, painful, stains the skin and less absorbed so IV injection whether by repeated small doses or infusion in saline solution is preferable.
    IV therapy may be complicated by flushing, urticaria, arthralgia, fever, lymphadenopathy, phlebitis and anaphylaxis.
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  • 17. Treatment
    Packed RBCs: is used if more rapid response is needed e.g. pre-operative.
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  • 18. MegaloblasticAnaemia
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  • 19. MegaloblasticAnaemia
    It is caused by deficiency of folic acid and / or vitamin B12.
    Daily Requirement:Normalfolate requirement is 500 mg /day and a similar amount is needed during pregnancy so that the daily requirement during pregnancy is 1mg.
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  • 20. MegaloblasticAnaemia
    Folic Acid Deficiency Anaemia
    It is uncommon.
    Daily Requirement:
    Normal folate requirement is 500 mg /day and a similar amount is needed during pregnancy so that the daily requirement during pregnancy is 1mg.
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  • 21. MegaloblasticAnaemia
    Folic Acid Deficiency Anaemia
    Aetiology:
    * Inadequate intake.
    * Defective absorption.
    * Increased demand e.g. pregnancy.
    * Drugs: folic acid antagonists as epanutin (anti-epileptic).
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  • 22. MegaloblasticAnaemia
    Folic Acid Deficiency Anaemia
    Clinical Picture:
    * General symptoms of anaemia (see before).
    * GIT manifestations in the form of:
    > dyspepsia,
    > anorexia,
    > nausea,
    > vomiting,
    > diarrhoea,
    > beefy (red, glassed) tongue,
    > hepatosplenomegaly.
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  • 23. MegaloblasticAnaemia
    Folic Acid Deficiency Anaemia
    Investigations:
    * Blood film:
    > Macrocytichyperchromic RBCs.
    >Hypersegmentedneutrophilic nuclei (>5 lobes).
    * Serum folate level: is low measured by radioimmunoassay.
    * Bone marrow: abnormal red cell precursors (megaloblasts).
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  • 24. MegaloblasticAnaemia
    Folic Acid Deficiency Anaemia
    Treatment:
    * Diet rich in folic acid as liver, kidney and meat.
    * Folic acid 5-15 mg /day orally.
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  • 25. MegaloblasticAnaemia
    Vit. B12 Deficiency Anaemia (Addisonian Pernicious Anaemia):
    It is rare.
    Daily Requirement: less than 1mg.
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  • 26. MegaloblasticAnaemia
    Vit. B12 Deficiency Anaemia (Addisonian Pernicious Anaemia)
    Aetiology:
    * Inadequate intake (rare).
    * Deficient intrinsic factor as in atrophic gastritis or gastrectomy.
    * Malabsorption syndrome.
    * Increased demand e.g. pregnancy.
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  • 27. MegaloblasticAnaemia
    Vit. B12 Deficiency Anaemia (Addisonian Pernicious Anaemia)
    Clinical Picture:
    * General symptoms of anaemia.
    * GIT manifestations: as folic acid deficiency.
    * Nervous manifestations:
    >Subacutecombined degeneration.
    > Peripheral neuritis.
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  • 28. MegaloblasticAnaemia
    Vit. B12 Deficiency Anaemia (Addisonian Pernicious Anaemia)
    Investigations:
    As folic acid deficiency + decreased serum vit. B12.
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  • 29. MegaloblasticAnaemia
    Vit. B12 Deficiency Anaemia (Addisonian Pernicious Anaemia)
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  • 30. MegaloblasticAnaemia
    Vit. B12 Deficiency Anaemia (Addisonian Pernicious Anaemia)
    Treatment:
    >Vit. B12 IM injection.
    >N.B. Folic acid is never given alone for B12 deficiency anaemia as it will increase the nervous manifestations.
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  • 31. HaemolyticAnaemias
    Congenital (Intracorpuscular):
    A. Spherocytosis.
    B. Haemoglobinopathies
    C. Glucose -6- phosphate dehydrogenase deficiency (G-6-PD).
    Acquired (Extracorpuscular):
    A.Chemicals: e.g. drugs, lead and snake venum.
    B.Infections: e.g. malaria and clostridium welchii.
    C.Hypersplenism.
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  • 32. HaemolyticAnaemias
    B. Haemoglobinopathies
    a. Thalassaemia:
    > a - thalassaemia Major.
    > a - thalassaemia Minor.
    > ß - thalassaemia Major.
    > ß - thalassaemiaMinor
    b. Sickle cell anaemia.
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  • 33. Congenital Spherocytosis
    An autosomal dominant disorder in which there is deficiency in the lipoprotein of cell membrane leading to increased rigidity of the RBCs and hence its destruction especially in the spleen.
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  • 34. Congenital Spherocytosis
    >Features of anaemia (see before).
    >Features of haemolytic jaundice:
    o Lemon yellow skin,
    o ting of jaundice in the sclera,
    o dark stool and normal urine which darkens on standing.
    >Hepatosplenomegaly: are common.
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  • 35. Congenital Spherocytosis
    The condition is inherited by 50% of the mother offspring. In the infant, jaundice develops within 48 hours of birth and exchange transfusion may be required.
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  • 36. Thalassaemia
    An autosomal inherited disorder resulted from failure of production of either a chain (a- thalassaemia) or ß chain (b -thalassaemia) of the haemoglobin molecule and their replacement with other polypeptide chains.
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  • 37. Thalassaemia
    >a- thalassaemia:
    a- thalassaemia major (homozygotes):
    a- thalassaemia minor (heterozygotes):
    >ß-Thalassaemia
    ß-thalassaemia major (homozygotes):
    ß-thalassaemia minor (heterozygotes):
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  • 38. Thalassaemia
    a- thalassaemia major (homozygotes):
    The foetus with this disorder is affected in utero showing polyhydramnios, erythroblastosis, anaemia and hydrops resembling Rh-incompatibility.
    This foetus does not survive due to inability of oxygen transfer as the a-chain is responsible for O2 carrying capacity.
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  • 39. Thalassaemia
    a- thalassaemia minor (heterozygotes):
    Patient develops mild progressive anaemia during pregnancy.
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  • 40. Thalassaemia
    ß-thalassaemia major (homozygotes):
    The disorder starts in childhood leading to death of the patient mostly in the 2 nd or 3rd decade.
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  • 41. Thalassaemia
    ß-thalassaemia minor (heterozygotes):
    As a- thalassaemia minor.
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  • 42. Thalassaemia
    Effect on pregnancy:
    * ß-Thalassaemia major is rarely encountered in pregnant women, but if this happened the prognosis is poor.
    * Anaemia becomes severe in mid-pregnancy and may result in heart failure.
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  • 43. Sickle Cell Anaemia
    An autosomal inherited disorder in which glutamic acid in position 6 of the b - chain of the haemoglobin molecule is replaced by valine. This leads to production of HbS. Hb S on exposure to hypoxia forms insoluble aggregations and RBCs become sickle-shaped and are subsequently fragmented.
    In addition, these sickle-shaped cells increase the blood viscosity and occlude blood vessels of various organs.
    The manifestations appear usually in homozygous not in heterozygous.
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  • 44. Sickle Cell Anaemia
    Clinical picture:
    * Feature of anaemia and haemolytic jaundice.
    * Multiple infarcts due to obstruction of microcirculation in the spleen, kidney, CNS, retina, bone, lungs and heart.
    * Increased susceptibility to infections especially urinary.
    * Attacks of severe abdominal pain and fever are common due to ischaemia and infarctions.
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  • 45. Sickle Cell Anaemia
    Clinical picture:
    * Pre-eclampsia like- syndrome with hypertension, oedema and proteinuria may develop.
    * Increased foetal wastage from abortion, preterm labour and growth retardation associated with placental insufficiency due to maternal placental bed thrombosis.
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  • 46. Sickle Cell Anaemia
    Management of sickle cell disease during labour:
    * Avoid: hypoxia, dehydration and acidosis.
    * Treat crises by: rehydration, bicarbonate, analgesic, heparin or low molecular weight dextran.
    * Prophylactic antibiotic.
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  • 47. Investigations of HaemolyticAnaemia
    Serum bilirubin: raised.
    Urine: increased urobilinogen.
    Stool: increased stercobilinogen.
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  • 48. Investigations of HaemolyticAnaemia
    Blood film:
    shows normocyticnormochromicanaemia and;
    o Small spherical RBCs in case of spherocytosis.
    o Target cells in case of Thalassaemia major.
    o Sickling after inducing hypoxia by addition of Na bisulphite in case of sickle cell anaemia.
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  • 49. Investigations of HaemolyticAnaemia
    * Electrophoresis: detect type of haemoglobin in haemoglobinopathies.
    * Estimation of glucose-6-phosphate dehydrogenase activity.
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  • 50. Treatment of HaemolyticAnaemia
    * Blood transfusion: in acute attacks.
    * Folic acid and iron therapy: may be indicated.
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  • 51. Treatment of HaemolyticAnaemia
    * Splenectomy: may be beneficial in spherocytosis and some cases of thalassaemia major, but not to be done during pregnancy.
    * Avoid precipitating factors: as hypoxia in spherocytosis and oxidative agents in G-6-PD deficiency.
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