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Management of pregnancies at risk of HDN3. Management of pregnancies at risk of HDNI. Treatment In the motherPlasma exchange Intensive plasma exchange in women immunized to the D antigen leads to lowering of anti-D levels. Intravenous immunoglobulin Administration of intravenous immunoglobulin to the mother during pregnancy decreases disease severity both with and without concomitant plasmapheresis. The requirement for intrauterine transfusions and early delivery is reduced. Mechanism Intravenous immunoglobulins act by blocking receptors on foetal macrophages and placental trophoblastic cells by - Feedback suppression of antibody synthesis - Blocking the placental transfer of antibody to the foetus Premature delivery The gestational age at which 50% of all stillbirths due to haemolytic disease occurs is after 33-35 weeks. With better facilities available for the care of prematurely delivered infants, premature induction is recommended after 33 weeks. II. Management of foetus Intrauterine transfusion (IUT) This is the method of choice for a) infants with severe disease at 33 weeks gestation (upper zone or middle zone 2 of Lieley’s graph) b) foetus with survival chance by premature induction of less than 6%. Intraperitoneal transfusion (IPT) Red cells are injected into the peritoneal cavity of the foetus from where they are taken into the blood stream. Intravascular transfusion (IVT) This is performed through a needle inserted into the umbilical vein under ultrasonographic control. Packed red cells are infused at a rate of to 10 ml per minute until a total of 50 ml per kg has been given. Selection of blood for IVT Blood used for intrauterine transfusion should be : * less than 72 hours old * Group 0 * D negative * Cross matched with the mother’s serum * Haematocrit (Hct.): - Female donors: 125 g/l or 7.8 mmol/l (min. Hct = 0.38) - Male donors: 135 g/l or 8.4 mmol/l (min. Hct = 0.4) * Irradiated to avoid GVHD * Leucodepleted to avoid alloimmunization * Adequately tested and screened for transfusion transmitted infections including CMV III Management of the infant Severe hyperbilirubinaemia may develop in infants, even in those who have received intrauterine transfusion leading to brain damage and death oif not managed early. Exchange transfusion is the most important management for neonates with hyperbilirubinaemia. Exchange transfusion acts by * Correcting the anaemia * Preventing hyperbilirubinaemia * Removing the maternal antibodies present * Remoivng the sensitized red cells Principle Small volumes of the infant’s blood are removed and are replaced by fresh blood. A transfusion equivalent to two times the blood volume (180 ml/kg) replaces 90% of the infant’s red cells by donor cells. Indications of exchange transfusion 1. Moderately and severely affected neonates Cord haernoglobin < 13 g/dl or a bilirubin level > 4 mg/dl (3.5 mg/dl in premature infants) 2. Rapid rate of rise of bilirubin If the serum bilirubin level exceeds 20 mg/dl, an exchange transfusion should be performed. 3. Severe anemia Selection of blood for ET Blood used should be ABO compatible; Rh (0) negative; Irradiated, if possible; Plasma reduced; Hct, as fresh as possible (48 his) or less than 4 days old and adequated tested. Rationale for using fresh blood i) When blood is fresh, the fall in platelets is minimal. Ii) Red cells stored for long begin to loose potassium with resultant hyperkalemia. iii) Stored blood Loses 2,3 DPG, as a result the blood is less ale to deliver âxygen to the tissues. Compatibility testing for ET 1. The R.B.C. should be compatible with the mother’s serum by antiglobulin and enzyme technique. 2. If mother’s blood is not available, baby’s serum or the eluate from cord cells is used. Prevention of Rh HDN Rh immunization can be prevented by administration of anti-D gamma globulin within 72 hours after delivery. Accordingly, all Rh negative women should be administered anti-D immunoglobulin following Rh positive delivery, abortion, amniocentesis or tubal pregnancy. Dose The standard dose is 25 ug per ml cells i.e. 300 ug anti-D. Antenatal administration of anti-D. Antenatal immunoprophylaxis i.e. administration of anti-D in the Rh(D) negative mothers after the 28th week of gestation, can further reduce the frequency of anti-D immunization. Haemoiytic Disease due to other Rh Antibodies After anti-D, anti-c is the second most common Rh antibody associated with severe HDN. About 75% females get immunized to cantigen during pregnancy and the rest 25% following transfusion. About 90% of c+infants born to mother with anti-c can be affected. As only R1R1 (CDe/CDe) persons form this antibody, incidence can be reduced if Ri Ri women are given R1R1 blood. HDN due to anti-C, anti-E and anti-e can occur but is usually uncommon and mild in severity. ABO Haemolytic Disease ABO haemolytic disease is limited to mothers of blood group 0 with babies of blood group A or B. Incidence The association of group 0 mothers with A or B group babies occurs in 15% of all pregnancies. Evidence of incompatibility is observed in only 3% of pregnancies and still fewer infants require exchange transfusion. Maternal antibody Mothers are usually of group 0 as igG anti-A and anti-B occur much more frequently in group 0 than in group B and A mothers. ABO-HDN tends to occur in newborns whose mothers have high levels of IgG antibody. The methods used to detect the antibody are: 1. Antibody aétivity after neutralization with A or B blood group substance present in saliva. 2. Denaturatlon of igN using 2-mercaptoethanol 3. Indirect antiglobulin technique 4. Haemolytic activity The diagnosis of ABO-HDN depends primarily on the serological findings in the newborn., Clinical features The clinical features observed in ABO-HDN are - Hyperbilirubinaemia commending within 24 hours of bith - Mild anaemia with reticulocytosis SerologIcal tests in the newborn Direct antlglobulin test Mildly affected infants may be negative by DAT. Wtih the use of sensitive techniques, some anti- A or anti-B can be detected in all affected infants. The foetal erythrocytes have weaker expression of A or B sites. This explains the weakly reactive DAT as fewer anti-A molecules are bound firmly to the cell due to the great distance betweent he A sites. Eluate Antibodies eluted from these cells react strongly with adult A red cells in which the A sites are more numerous and therefore closer to one another. Diagnosis Infant 1. DAT positive 2. Mild anaemia, reticulocytosis and normoblastaemia 3. Microspherocytosis in blood films 4. Hyperbilirubinaemia Mother 1. Serum contains high levels of anti-A and/or anti-B antibody of IgO type. Management of AlSO haemolytlc disease 1. Exchange transfusion It is rarely required as severe anaemia is uncommon. Severe hyperbilirubinaemia, if occurs is the main indication for ET. If performing exchange transfusion, always use 0 group blood in ABO-HDN. 2. Phototherapy If the serum bilirubin tends to rise, phototherapy may be helpful in controlling it. Phototherapy should be given if the serum bilirubin reaches 12 mg/dl within 18 horus or 14 mgI dl within 24 hours. Other Antibodies Causing HDN Anti-Kell : Anti-K can be detected in 1 per 1000 pregnant women. HDN due to anti-K is not frequent as most infants are K negative. A history of previous transfusion is usually elicited. Anti-K has a disproportionate effect on red cell precursors, causind more anaemia and less jaundice. There is a poor correlation between disease severity and the titre of antibody in the maternal serum. Anti-Fya and anti-Jka can also cause severe HDN. HDN due to anti-K, anti-Jkb, anti-M, anti-S, anti-s can occur although it is unusual or even rare. Anti-Lea, anti-Leh, anti-I, anti-HI and anti-Pi are naturally-occurring cold antibodies and do not cause HDN.
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