Hemolytic disease of the newborn - Pathogenesis of Rh negative fetuses tasks with Rh positive

I. Transition fetal red blood cells (loaded with antigen D) in maternal circulation
 The transition takes place largely at birth and the last two months of pregnancy (after 32-35 weeks)Feto-maternal hemorrhage can occur and the year the first two months pregnancy either spontaneously or in ectopic pregnancy or during pregnancy if obstetric practice maneuvers for diagnostic purposes (trophoblastic puncture, early amniocentesis).The volume of fetal hemorrhage into maternal circulation is generally lower: 0.25 ml at birth (rarely more than 5 ml).Small volumes are yet to produce a response capapile primary or anamnestic. Massive hemorrhage (50 ml) sun possible in case of fetal death (stillborn).The volume of fetal hemorrhage into maternal circulation can Kleihauer-Betke test quantified by.
 II. AntiRh secretion of maternal antibodies (anti-D)
 The Rh system antibodies no natural (as in ABO system).Immune response involves two exposures of the mother to the D antigen (Rh)
a) first exposure triggers primary answer: D antigen is taken up and processed by macrophages and transferred to clone B-lymphocytes with specific receptors D, B lymphocytes with memory "sensitized" remains stuck in the lymphoid tissues. A very small number of B lymphocytes become plasma cells secreting antibodies to very low (infraserologic).Primary response can be blocked by immunoglobulin antiD
b) second exposure triggers immunological conflict.D antigen (fetal) macrophages and avoids direct contact with B lymphocytes specific memory. It stimulated both proliferation (increased number of lymphocytes B in clone) and their transformation into plasma cells secreting rate of IgG antibodies.Anamnestic response can be triggered by very small volumes of fetal blood (0.2 to 1 ml) and can not be blocked by immunoglobulin antiD.
AntiD antibodies (Rh) are both IgM (high molecular weight, transient, shown in saline environment) and IgG (molecular weight, persistent, highlight the environment albumin).IgG antibodies are produced mainly in the second half of pregnancy.
Practical implications of how the immune response of Rh incompatibility in Maternal-Fetal are:1. feto-neonatal hemolytic disease occurs in pregnant women not primigeste, primiparous (Ig, Ip);2. antiRh antibody level (D) increases with successive tasks;3. antiD antibody level increases with age pregnancy;4. Rh negative woman, once immunized, immunized remains for life and will make antibodies to any task antiRh with Rh-positive fetus;5. If a woman has not been immunized Rh negative in second pregnancy with Rh positive fetus is unlikely to longer immunized.
Pregnant IgIp can, however, to be immunized during pregnancy antiRh in the following situations:- If they receive Rh-positive blood transfusions precinceptual in a moment of their lives (a unit of blood adult primary response occurs in 80% of cases);- If cause feto-maternal hemorrhage than in the first two months of pregnancy (by puncture trophoblastic or early amniocentesis) and in the last two months of pregnancy (spontaneous, toxemia pregnant cerclage, uterine, off the placenta).
Frequency Rh immunization of pregnant women with Rh negative with positive daughter is only 5% (no passage or passage in fetal blood flow decreased maternal, fetal antigen on the red reprezantat Dslab; shorter lifetime in the incompatibility of fetal erythrocyte ABO).
 III. Switching maternal immune antibodies (IgG) in the fetus with the onset of haemolysis (extravascular)
 Antibodies are found in fetal circulation in two forms: free (serum) and absorbed on the surface of red blood cells (may direct Coombs test degelati by)Red blood cells "wrapped" antibodies have shorter lifespan, are taken from circulation by macrophages (especially spleen) and destroyed (lysed) extravascular.The result is anemia and hyperbilirubinemia hiperhemolizei extravascular.