Laboratory Monitoring of Mother, Fetus, and Newborn in Hemolytic Disease of Fetus and Newborn

Abstract

<b><i>Background:</i></b> Laboratory monitoring of mother, fetus, and newborn in hemolytic disease of fetus and newborn (HDFN) aims to guide clinicians and the immunized women to focus on the most serious problems of alloimmunization and thus minimize the consequences of HDFN in general and of anti-D in particular. Here, we present the current approach of laboratory screening and testing for prevention and monitoring of HDFN at the Copenhagen University Hospital in Denmark. <b><i>Summary:</i></b> All pregnant women are typed and screened in the 1st trimester. This serves to identify the RhD-negative pregnant women who at gestational age (GA) of 25 weeks are offered a second screen test and a non-invasive fetal RhD prediction. At GA 29 weeks, and again after delivery, non-immunized RhD-negative women carrying an RhD-positive fetus are offered Rh immunoglobulin. If the 1st trimester screen reveals an alloantibody, antenatal investigation is initiated. This also includes RhD-positive women with alloantibodies. Specificity and titer are determined, the fetal phenotype is predicted by non-invasive genotyping based on cell-free DNA (RhD, K, Rhc, RhC, RhE, ABO), and serial monitoring of titer commences. Based on titers and specificity, monitoring with serial peak systolic velocity measurements in the fetal middle cerebral artery to detect anemia will take place. Intrauterine transfusion is given when fetal anemia is suspected. Monitoring of the newborn by titer and survival of fetal red blood cells by flow cytometry will help predict the length of the recovery of the newborn.

Non-Invasive Fetal K Status Prediction: 7 Years of Experience

“…In 100% of the results of a KEL * 01.01 prediction the results have been useful to the clinicians. In case of a predicted KEL * 01.01 -negative fetus the woman should appear in week 25 and 32 for ultrasonographic scans, titer determination, and antibody screen for the occurrence of additional antibody specificities [ 27 ]. Depending on specific high-risk circumstances, an extra ultrasonographic scan and titer determination can be done around GA 16–18 weeks.…”

Hemolytic disease of the fetus and newborn: systematic literature review of the antenatal landscape

“…Despite advances in the prevention of pregnancy-related red blood cell immunization and management and treatment of pregnancies affected by hemolytic disease of the fetus and newborn (HDFN) over recent decades, the disease still poses a significant risk in affected pregnancies [ 1 , 2 ]. HDFN is caused by maternal alloimmunization through exposure to incompatible red blood cell antigens of the fetus or through incompatible blood transfusion [ 1 , 3 ]. The then-formed immunoglobulin G (IgG) antibodies are actively transported across the placenta and can cause fetal hemolysis and anemia.…”

“…Additionally, the disease still poses a significant risk for mortality and morbidity in developing countries, whereas it is considered treatable with good outcomes in developed countries. Serological monitoring, ultrasonography, and Doppler imaging decreased the need for risky and invasive diagnostic procedures [ 3 , 8 – 12 ]. Antenatal treatment, however, still relies predominantly on (often serial) intrauterine transfusion (IUT)—an invasive procedure that carries maternal and fetal risks [ 13 , 14 ].…”

Anti Colton-A Foeto-Neonatal Haemolytic Disesase: Diagnosis; Clinical Outcome and Family Study

“…Clinically significant red cell alloantibodies are those that have the potential to cause haemolysis of red cells bearing the corresponding antigen [1]. Maternal antibodies capable of causing HDFN could either be ABO or non-ABO alloantibodies [3,4]. If a major incompatibility between mothers and their newborns occurs, so mothers with an O blood group may form IgG-class antibodies against A and B antigens, which could pass across the placenta and lead to a variable degree of HDFN.…”

“…These antibodies form when foetal erythrocytes that express certain RBC antigens that are not expressed in the mother cross the placenta and gain access to maternal blood. Non-ABO HDFN usually occurs in pregnancies following the first which serves as an immunizing event [3,4]. This antibody response may be sufficient to destroy foetal red cells leading to haemolysis, the release of bilirubin, and anaemia.…”