Anaemia in pregnancy


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Anaemia in pregnancy

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