fetal health

Fetal Erythroblastosis Symptoms

Definition

Fetal erythroblastosis is a form of haemolytic anemia due to transplacental transmission of maternal antibodies directed against the red blood cells of the fetus or newborn.

This pathology is usually caused by an incompatibility of the Rhesus factor (or Rh: antigen expressed on the surface of the red blood cells), which induces a fetal erythrocytic hyper-education. Erythroblastosis can develop, in particular, when an Rh-negative woman is fertilized by a Rh-positive man and conceives an Rh-positive fetus.

As a rule, fetal erythrocytes cross the placenta and pass into the maternal circulation throughout pregnancy, stimulating the production of maternal antibodies against the child's Rh factor; this "exchange" is maximum towards the end of gestation and at the time of birth. In the pregnancy following the "sensitizing" one, if the Rh-negative woman conceives a child with Rh-positive blood, the maternal antibodies reach the fetus through the placenta and cause the lysis of the red blood cells.

Other causes of maternal production of anti-Rh antibodies are injection with needles contaminated with Rh-positive blood and involuntary transfusion of Rh-positive blood.

Fetal erythroblastosis may also arise from the involvement of other antigens, as in the case of the Kell or Duffy system. The maternal-fetal incompatibilities of AB0 blood groups, which cause this phenomenon, on the other hand, are less severe and less frequent than those of the Rh factor.

Most common symptoms and signs *

  • Miscarriage
  • anasarca
  • Anemia
  • anisocytosis
  • Ascites
  • asphyxiation
  • Asthenia
  • Cardiomegaly
  • Dyspnoea
  • Edema
  • Hepatomegaly
  • Hydrops Fetal
  • Jaundice
  • Fetal death
  • Pallor
  • Polyhydramnios
  • Muscle spasms
  • splenomegaly
  • Pericardial effusion
  • Pleural effusion

Further indications

Fetal erythroblastosis causes clinical pictures of varying degrees. No complications develop during the initial sensitizing pregnancy; however, in subsequent gestations, maternal antibodies cross the placenta and hemolyze fetal erythrocytes, resulting in anemia. In an attempt to correct the latter, fetal bone marrow produces and releases immature red blood cells (erythroblasts) in the peripheral circulation (fetal erythroblastosis). This event can be so severe as to cause fetal intrauterine death due to high-range heart failure. Due to haemolytic-type anemia, asphyxia often occurs during labor and delivery, so caesarean section is usually indicated.

After birth, newborns suffering from fetal erythroblastosis are extremely pale and have generalized edema, hypoproteinemia and pleural and peritoneal effusions. Immediately after delivery, affected children usually have elevated levels of indirect bilirubin (hyperbilirubinemia), which can cause nuclear jaundice, due to the continuous haemolytic effect of anti-Rh antibodies that have passed the placental filter.

Erythroblastosis also predisposes to respiratory distress syndrome.

At the first prenatal visit, all women must be screened for blood group and HR, and in search of antigens and maternal antibodies that can cause fetal erythroblastosis. Diagnostic tests may also require serial measurements of the maternal antibody titre (to be measured monthly until week 24, then every 2 weeks), paternal screening and, based on the estimated severity of the disease, fetal tests.

The treatment of erythroblastosis may include intrauterine fetal blood transfusions (by injecting the Rh– blood directly into the fetus, via the mother's abdominal wall, even every two weeks until delivery) or the neonatal exanguino-transfusion. With this last procedure, the child's blood is replaced almost completely with another one, provided by donors, without the specific antibodies against the Rh factor. In any case, the birth must be the least traumatic possible. Manual removal of the placenta should be avoided, as it can force fetal cells into the maternal circulation.

Maternal sensitization and the production of antibodies caused by RH fetal incompatibility can be prevented by administering immunoglobulin Rh0 (D) to women at risk. This preparation contains high titres of anti-Rh antibodies which neutralize the Rh positive fetal red blood cells.