See ((Rh hemolytic disease))
Pregnancy complicated by red blood cell alloimmunization.
Alloimmunization can occur when fetal cells bearing a foreign antigen to the mother enters the maternal circulation.
Red cell alloimmunization is typically caused through exposure, during pregnancy, to fetal red cell antigens, which trigger antibody production.
As little as 0.1 mL RhD positive blood is enough to cause sensitization in a Rh negative woman.
Hemolytic disease of the fetus and newborn results from maternal fetal erythrocyte antigen incompatibility and transplacental transfer of maternal antierythrocyte antigen IgG alloantibodies, which causes fetal hemolytic anemia.
The risk of fetomaternal hemorrhage is low in the first two trimesters, but increases in the third trimester, and at the time of delivery 50% women have sufficient fetomaternal hemorrhage to be at risk for sensitization.
Early onset, severe hemolytic disease of the newborn occurs at 24 weeks, gestation or earlier, and is associated with substantial fetal and neonatal, morbidity and mortality.
Fetal hemolysis results in severe fetal anemia, and even hydrops fetalis, which is an abnormal accumulation of fluid in at least two fetal compartments, which is treated with intrauterine transfusion.
Fetomaternal hemorrhage and maternal sensitization can be increased by previous abortions, ectopic pregnancies, and invasive procedures including amniocentesis and chorionic villus sampling.
Alloimmunization can occur only if the mother is negative and the fetus is positive for the Rh antigen.
Fetal Rh hemolytic disease anemia may lead to fetal death as early as 17 weeks gestation.
Survival rates exceed 90% if anemia diagnosed and treated with intrauterine blood transfusions.
Intrauterine transfusion is technically challenging, especially at early gestational ages, with an incident of complications of 2.7% per procedure.
Such complications include fetal bradycardia, and stillbirth.
Anemia severity identified by mother’s obstetrical history and serum antibody levels.
Pregnant women are routinely screened early in the first trimester for alloantibodies.
If screening is negative and the fetus is RhD positive primary prophylaxis with anti-D immune globulin is administered to the pregnant female in situations that pose a risk of fetal maternal hemorrhage.
Administration of IgIV in addition to phototherapy results in reduced hemolysis and the need for exchange transfusion.
If the alloantbody screening is positive and titer and type of antibody indicates a risk of fetal anemia, the peak systolic velocity in the middle cerebral artery is monitored with Doppler ultrasound throughout pregnancy.
Velocity exceeding 1.5 times the median value of fetus at the same gestational age indicates the presence of moderate to severe fetal anemia, warranting intrauterine transfusion.
Routine anti-RhD prophylaxis has reduced RhD alloimmunization,, but early onset, severe hemolytic disease persists, owing to missed administration and lack of prophylaxis for non-RhD antigens.
In a study of patients with high risk for hemolytic disease of the newborn in early gestation treated with a monoclonal antibody nipocalimab delayed the timing of the first transfusion as compared with standard secondary preventive options.
Nipocalimab target is the neonatal Fc receptor the only known transplacental IgG transporter.
Symptoms and signs in the newborn:
Anemia that creates the newborn’s pallor.
Jaundice or yellow discoloration of the newborn’s skin, sclera or mucous membrane.
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This may be evident right after birth or after 24–48 hours after birth.
This is caused by bilirubin.
Enlargement of the newborn’s liver and spleen.
The newborn may have severe edema of the entire body.
Dyspnea or difficulty breathing.
Standard of care is to monitor high risk pregnancies for fetal anemia by means of the middle cerebral artery Doppler ultrasound and fetal blood sampling, foowedvby timely intrauterine transfusions to avoid fetal hydrops and pregnancy loss.
Complications of intrauterine transfusion include fetal death, pre-term gestation, pre-term rupture of membranes, and pre-term birth.
Early intrauterine transfusion is associated with very high risk of perinatal loss at 17% per procedure less than 20 weeks gestation.
Ante-natal treatment with IV immune globulin with or without plasmapheresis delays uterine transfusion but is still associated with poor pregnancy outcomes.
In patients with the criteria for very severe red cell allohumanization intrauterine transfusion can be postponed through the use of therapeutic plasma exchange, polyvalent intravenous immune,,globulin, or both.
Nipocalimab is a neonatal FC receptor blocker for the deferment of multiple IgG auto antibody or allo antibody driven diseases.
Nipocalimab treatments delay will prevent fetal anemia or intrauterine transfusions as compared with the historical benchmark in pregnancies at high risk for early onset, severe hemolytic disease of the newborn.