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isoimmunisation

William 2001. isoimmunisation. Fetal anemia Fetomaternal hemorrhage Isoimmunisation Immune hydrops Management Pervention Large fetomaternal Hge. Normal fetal Hb % > 35 weeks = 17 gm/ dL Fetal anemia = < 14 gm/ dL Causes : Placenta cut or torn Fetal vessel perforation

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isoimmunisation

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  1. William 2001 isoimmunisation

  2. Fetal anemia Fetomaternal hemorrhage Isoimmunisation Immune hydrops Management Pervention Large fetomaternalHge

  3. Normal fetal Hb% > 35 weeks = 17 gm/dL Fetal anemia = < 14 gm/dL Causes: • Placenta cut or torn • Fetal vessel perforation • Raising the neonate above the abdomen of his mother before clamping the cord Delayed clamping of the cord  ↑ of fetal Hb by 20% Fetal anemia

  4. Common in all pregnancies Rarely > 30mL = 0.3 – 0.6% Benefit in fetal karyotyping Keihauer – Batke test: Identify fetal RBCs by acid elusion  darker than maternal RBCs Rosette test: Maternal blood + anti D Ab+ indicator  fetal blood surrounded by Abs More accurate in hemoglobinopathy Fetal-to-maternal hemorrhage

  5. Severe anemia sinusoidal FHR not pathognomonic  evaluate immediately Chronic anemia may  normal FHR Significant acute /chronic Hgemay  Neurological impairment due to: Hypotension  ↓ perfusion  Ischemia  CNS infarction Obstetric management may not improve CNS damage

  6. Large fetal Hg may  fetal death in 5% and the cause may be unknown e.g. chorioangioma Placental abruption : usually  mild Hg except if traumatic Quantification of volume of blood loss: • influence management • Determine the dose of Anti D Ig

  7. Fetal red cells = maternal Hct X maternal blood volume X % of fetal cells in Kleihauer - Batke test ÷ neonatal Hct Causes of fetal-to-maternal Hg: • Early abortion • Elective abortion

  8. Ectopic • Amniocentesis • Cordocentesis • Chorionic villous sampling • Antepartum trauma • Placental abruption • Fetal demise • Manual placental extraction • External version

  9. isoimmunisation

  10. ABO blood group • CDE blood group • Other blood groups • Kell antigen • Other antigens

  11. History: 1892 Ballantin hydropsfetalis 1932 Anemia and reticulosis are present in hydropsfetalis 1940 Landsteiner & Weiner  Rh factor 1941 Levein  hydrops is caused by maternal isoimmunisation by Rh –ve fetus 1961 Anti Rh

  12. - Fetal blood contain > 400 Ags most of them are insignificant - Most people inherit at least 1 Ag from their fathers that is lacking in their mothers - Isoimmunisation of an Rh –ve pregnant woman occur as a result of: Rh +ve fetus Blood transfusion

  13. Isoimmunization is rare because: • Variable Ag amounts • Variable antigenicity • Maternal immune respond • ↓ placental passage • ABO incompitability destruction of fetal RBCs

  14. Not all isoimmunization hydrops 2% of all women are isoimmunized 6 months postpartum % of isoimmunisation with Rh-ve ABO compatible fetus: 2% at delivery 7% 6 months postpartum 7% next pregnancy Total = 16%

  15. ABO blood group incompatibility: - The most common cause of hemolytic disease of the neonate - 20% of all fetuses are ABO incompatible only 5% of them are clinically affected -  Mild anemia & ↑ reticulocytes - No erythtoplastosis - Treated by phototherapy

  16. Difference from Rh incompatibility: • Affect 1st baby • Milder ( Ig M does not pass placenta) • Rarely progressive • Affect African Americans Criteria of ABO incompatibility: • 1st day jaundice • Mother O, fetus A,B,or AB group • Anemia, ↑ reticulocytes

  17. Management of ABO incompatibility: Same as Rhisoimmunization but: • No amniocentasis • No blood transfusion Because there is no hydrops CDE blood group: 5 types: c, C, e, E, D

  18. - D is +ve if present and –ve if absent - D isoimmunisation is the most common isoimmunization - D –ve pregnant women are sensitized if their fetus is D +ve - CDE genes are inherited independent on other blood groups - They are located on chromosome 1

  19. Geographic distribution of D +ve populations: • Native Americans and Chinese 95% • African Americans 92% • Caucasians 87% • Basque 76%

  20. Other blood groups: % = 1 - ¼  Lewis blood group  mild jaundice starts weeks postpartum - 74% D, C, c, E & e antigens - Recently Rhisoimmunization is ↓ due to Anit D treatment - Now Rh = 40% Other Ags = 60%

  21. Kell antigen: - Caucasian kell +ve = 91% - Isoimmunisation occur by pregnancy or blood transfusion -  Much earlier and more severe anemia which can not be predicted by: • Maternal titer • AF bilirubin = mild/moderate

  22. - May  fetal death inspite of: Blood transfusion Normal AF bilirubin - Hemolysis ↓ due to: ↓ RBCs ↓ bilirubin - If maternal anti-KellAb titer ≥ 1 : 8  Cordiocentesis because AF bilirubin is out of proportion to anemia

  23. Other antigens: Kid Ag: Jk a –ve = 25% Jk b –ve = 25% Jk a - b +ve = 50% Duffy Ag: Fy a – b –ve in some blacks C Ag: Most common Ag after D  Moderate to severe hemolysis

  24. Immune hydrops

  25. Immune hydrops • Hyperbilirubinemia • Mortality • Identification of isoimmunization • Fetal Rh genotype

  26. RBCs hemolysis by isoimmunization  Hyperplasia of BM  Hyperplasia of extramedulary sites: Liver Spleen Liver: Fatty degeneration Deposition of hemosidrine Large canaliculi with bile Immune hydrops

  27. Heart: HF Lungs: Hge - immature When fluid accumulate in subcutanous tissues  hydropsfetalis Definition: Abnormal fluid in ≥ 2 sites: Ascitis – oedema – pleural effusion

  28. Placenta: • Enlarged cotyledons • Odemotusvilli • Boggy Fetus: • Dystocia due to: • Hepatospleenomegaly • Odema

  29. Heart: HF  hypoxia  capillary leakage Extramedularyhyperpleasia: Hepatic parynchemaldistruction  portal HTN  umbilical vein HTN Liver disease:  ↓ protein  ↓ colloidal osmotic P pathophysiology

  30. Study: Cordiocentesis in hydrops: • Hb = < 3.5 gm/dL • Plasma protein = < 2 SD • AF plasma protein ↑ The degree of anemia affect the degree of ascitis and made worse by ↓ plasma proteins

  31. Capillary endothelial damage:  Capillary leakage  ↓ protein Study: ↑ Umbilical vein pressure is due to cardiac dysfunction and not portal HTN Sinusoidal FHR = impending death

  32. Neonate: • Pale • Edematous • Limp • ↑ need for resuscitation • Dyspnea • Collapse • Hepatospleenomegaly • Petechiae • ecchymosis

  33. Less affected fetuses are born normal  jaundice within hours If untreated  kernicterus = CNS damage affecting basal ganglia Mortality: Reduced dramatically due to: • D Ig • Blood transfusion • Induction of labor hyperbilirubinemia

  34. Maternal serum Abs: Unbound to RBCs  disappear within 1 – 4 months  Indirect Coombs T Fetal serum Abs: Bound to RBCs  hemolysis  Direct Coombs test Neonatal blood group: Inaccurate because D-Ag may be coated with D-Ab Identification of isoimmunization

  35. If maternal Abs are present:  Ig G or Ig M ? (Ig M can not pass the placenta) If Ig G  antibody titer: < critical value 1 : 16  repeat > critical value 1 : 16  evaluate Critical values for other Ags: Kell ≥ 1 : 8 C, E ≥ 1 : 32

  36. The presence of Abs in the mother does not mean that: • The fetus is +ve • He will be affected Amnestic response: = ↑ Ab titer + Rh –ve fetus Because ½ of adult males are heterozygous for D Ag ¼ of women at risk are Rh -ve

  37. Estimation of fetal genotype: The father is tested for: • Blood group • Most likely arrangement of his CDE genes = presumed genotype based on the most common arrangement of genes in men of his race If the father is white: • 94% chance to be heterozygous • 47% chance of having D –ve fetus

  38. management

  39. Amniotic fluid evaluation • Expanded Liley graph • Fetal blood sampling • Subsequent child development • Other methods to ↓ hemolysis • Delivery • Exchange transfusion • Prevention • Routine antepartum anti-D

  40. ↑ Hemolysis ↑ AF bilirubin ↑ anemia Since AF bilirubin is very small  measured by a continuously recordingspectrophotometer and is demonstrable as a change in absorbance at 450 nm ( ∆ OD 450 ) then the results are plotted on Liley graph (1961) Amniotic fluid evaluation

  41. Zones of Liley graph: Zone 1 = mild anemia = 14 gm % Zone 2 = moderate/severe anemia = 13.9 – 8 gm % Zone 3 = severe anemia = < 8 gm % = death in 7 – 10 days Liley graph

  42. If the results are in zone 1 or 2: repeat in 1 – 2 weeks and draw a line between the 2 results: - If the trend of the line is: • Decreasing • Parallel to the lines of the graph = unaffected fetus or stable  repeat / 2 – 3 weeks until transfusion or delivery

  43. - If the trend of the line is: - Rising within the zone - Rising to zone 3 = Unstable  Managed as zone 3 If the results are in zone 3: = Severe anemia  Immediate blood transfusion or delivery

  44. Expanded Liley graph: Since Liley graph was made for fetuses > 27 week, expanded graph back to 18 – 20 weeks is inaccurate, because AF bilirubin < 25 weeks is high So, in cases of: • Hydrops < 25 weeks • Severe anemia < 25 weeks It’s better to do cordocentesis

  45. Cordocentesis is risky # amniocentesis Advantages: blood typing Recently amniocytesfor Rh typing: • 100% accurate • 99.7% sensitivity • 94% specificity • Also for C,E , Kell & other Ags Fetal blood sampling

  46. If fetus is Rh–ve no further tests If amniocentesis  possible anemia U/S  hepatomegaly NST/BPP  fetal stress  immediate blood transfusion or delivery

  47. Tests of cordocentesis: • Hb% • HTV • Indirect Coombs titer • Reticulocyte count Indications of IU blood transfusion: • Hb 2 gm/dL < mean of normal Hb in the fetuses in the same GA • HTV 30% = 2 SD < mean at all GAs

  48. Methods of intrauterine blood transfusion: Intraperitoneal- intraumbilical Subsequent child development: 90% normal – delayed - abnormal Other methods to ↓ hemolysis: • Plasmapheresis • Large dose of promethazine • Corticosteroids for immunosuppresion • D +ve erythrocytemembrane capsules All are ineffective

  49. Aim: = Delivery at or near term Monitor by fetal wellbeing tests If the fetus is very immature: Intrauterine blood transfusion If near term:  deliver • If lungs are mature  induce labor • If compromised fetus  CS delivery

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