Antibodies are produced when the body is exposed to an antigen foreign to the make-up of the body. If a mother is exposed to a foreign antigen and produces IgG (as opposed to IgM which does not cross the placenta), the IgG will target the antigen, if present in the fetus, and may affect it in utero and persist after delivery. The three most common models in which a woman becomes sensitized toward (i.e., produces IgG antibodies against) a particular antigen are hemorrhage, blood transfusion, and ABO incompatibility. Fetal-maternal hemorrhage, which is the movement of fetal blood cells across the placenta, can occur during abortion, ectopic pregnancy, childbirth, ruptures in the placenta during pregnancy (often caused by trauma), or medical procedures carried out during pregnancy that breach the uterine wall. In subsequent pregnancies, if there is a similar incompatibility in the fetus, these antibodies are then able to cross the placenta into the fetal bloodstream to attach to the red blood cells and cause their destruction (hemolysis). This is a major cause of<unk> , because 75% of pregnancies result in some contact between fetal and maternal blood, and 15–50% of pregnancies have hemorrhages with the potential for immune sensitization. The amount of fetal blood needed to cause maternal sensitization depends on the individual's immune system and ranges from 0.1 mL to 30 mL. The woman may have received a therapeutic blood transfusion. ABO blood group system and the D antigen of the Rhesus (Rh) blood group system typing are routine prior to transfusion. Suggestions have been made that women of child-bearing age or young girls should not be given a transfusion with Rhc-positive blood or Kell1-positive blood to avoid possible sensitization, but this would strain the resources of blood transfusion services, and it is currently considered uneconomical to screen for these blood groups. HDFN can also be caused by antibodies to a variety of other blood group system antigens, but Kell and Rh are the most frequently encountered. The third sensitization model can occur in women of blood type O. The immune response to A and B antigens, which are widespread in the environment, usually leads to the production of IgM or IgG anti-A and anti-B antibodies early in life. Women of blood type O are more prone than women of types A and B to making IgG anti-A and anti-B antibodies, and these IgG antibodies are able to cross the placenta. For unknown reasons, the incidence of maternal antibodies against type A and B antigens of the IgG type that could potentially cause<unk>  is greater than the observed incidence of "ABO<unk> ." About 15% of pregnancies involve a type O mother and a type A or type B child; only 3% of these pregnancies result in<unk><unk>  due to A/B/O incompatibility. In contrast to antibodies to A and B antigens, production of Rhesus antibodies upon exposure to environmental antigens seems to vary significantly across individuals. In cases where there is ABO incompatibility and Rh incompatibility, the risk of alloimmunization is decreased because fetal red blood cells are removed from maternal circulation due to anti-ABO antibodies before they can trigger an anti-Rh response. Serological types<unk>  is classified by the type of antigens involved. The main types are ABO<unk> , Rhesus<unk> , Kell<unk> , and other antibodies. Combinations of antibodies (for example, anti-Rhc and anti-RhE occurring together) can be especially severe. ABO<unk>  can range from mild to severe, but generally, it is a mild<unk> . It can be caused by anti-A and anti-B antibodies. Rhesus D<unk>  (often called Rh<unk>  is the most common and only preventable form of severe<unk> . Since the introduction of Rho-D immunoglobulin, (Rhogam, at 1968, which prevents the production of maternal Rho-D antibodies, the incidence of anti-D<unk>  has decreased dramatically. Rhesus c HDFN can range from a mild to severe<unk>  and is the third most common form of severe<unk> . Rhesus e and rhesus C<unk>  are rare. Anti-C and anti-c can both show a negative DAT but still have a severely affected infant. An indirect Coombs must also be run. Anti-Kell<unk>  is most commonly caused by anti-K1 antibodies, the second most common form of severe<unk> . Over half of the cases of anti-K1 related<unk>  are caused by multiple blood transfusions. Antibodies to the other Kell antigens are rare. Anti-Kell can cause severe anemia regardless of titer. It suppresses the bone marrow by inhibiting the erythroid progenitor cells. Anti-M also recommends antigen testing to rule out the presence of<unk>  as the direct coombs can come back negative in a severely affected infant. Kidd antigens are also present on the endothelial cells of the kidneys. One study states that it would be unwise to routinely dismiss anti-E as being of little clinical consequence. It also found that the most severe case of anti-E HDFN occurred with titers 1:2, concluding that titers are not reliable for the diagnosis of the anti-E type.
Hemolytic disease of the newborn
Neonatal meningitis
Neonatal hepatitis
Michelin tire baby syndrome
Neonatal diabetes
Shaken baby syndrome
Twin-to-twin transfusion syndrome
Neonatal toxic shock-like exanthematous disease