* The transplacental haemorrhage responsible for alloimmunization occurs mostly during childbirth; Sometimes it is favored in pregnancy by the following circumstances (placental abruption, ectopic pregnancy, intrauterine death, cervical cerclage, amniocentesis …).
These are generally the subsequent children will be achieved if Rh + as the first, severity of fetal hemolytic disease increases with the number of the child.
Placental passage of Acts is modest until the 20th SA, increases thereafter. Less than 0.1 ml of fetal erythrocytes Rh + may be sufficient to induce a primary immune response.
* Screening pregnant women is through the search for anti-erythrocyte irregular antibodies through indirect Coombs.Screening at birth is after collection of cord blood by direct Coombs.
* The assessment of the intensity of fetal hemolysis depends on several factors, the type of breast-Ac (anti-D, anti-c, anti-Kell), the early development of the Ag surface of the fetal red blood cell (Ag Rh and Kell are developed very early unlike those of ABO) and the importance of the step-wise transplacental which increases with gestational age.
* The sonographic signs of decompensation early fetal anemia: echogenic intestine, small blade of ascites, hepatomegaly most discreet pericardial effusion and a slight increase in the amniotic fluid.
* The study of RCF retrieves fetal distress (specific sinus rhythm with anemia, bradycardia).
Hydrops fetalis:
– Ultrasound: ascites, hepatomegaly, skin edema, polyhydramnios, and placental hypertrophy.
– Biology: hemoglobin <3 with thrombocytopenia, elevated transaminases, and erythroblastosis decrease in umbilical venous pressure of oxygen (O2 PV)
* The maternal anti-D alloimmunization 70% MFI screened at birth and 90% of serious IFM.
Anti-Kell alloimmunization are mostly transfusional, there is little risk of maternal-fetal incompatibility but fetal anemia induced by anti-Kell can be as severe early only with anti-D.
The maternal-fetal incompatibility in the ABO system are the most frequent and never cause severe intrauterine fetal disease. The MFI is to evoke in any neonatal jaundice in a child A or B mother O.
The Coombs test is negative.
* The primary prevention is to transfuse a patient with isogroupes products isorhésus and phenotyped.
* Prevention of pregnancy is immunization by injection of anti-D gamma globulin among all Rh negative woman who did not develop anti-D immunization after giving birth to an Rh-positive child after abortion during pregnancy during bleeding, after amniocentesis, a version, a strapping and other abdominal or pelvic trauma during pregnancy.modality: within 72 hours of the risk situation immunization, but it should give up to 72 hours if the time is exceeded.
* The Kleihauer: the count of fetal red blood cells in the maternal circulation.
Fetal erythrocyte 10 000 maternal red blood cells is the presence of 0.5 mL of fetal blood in the maternal circulation.
* Treatment: transfusion in utero; exchange transfusion in utero; plasmapheresis
– NB1: it is believed that ABO incompatibility mother-fetus reduces the risk Rhesus alloimmunization because the fetal red blood cells are rapidly destroyed.
– NB2: fetal, hematopoiesis begins around the 9th week of gestation, and is made in the liver and spleen; then in the bone marrow at 6 months.
– NB3: jaundice occurs only at birth; because during pregnancy bilirubin is excreted through the placenta.
