Erythroblastosis Fetalis: Causes, Signs and Symptoms, Diagnosis, Prevention, and Treatment
Introduction
Erythroblastosis fetalis, also known as Hemolytic Disease of the Newborn (HDN), is a potentially life-threatening condition in which a mother’s immune system attacks the red blood cells of her unborn baby. This condition occurs due to blood group incompatibility, most commonly Rh incompatibility, between the mother and the fetus. The destruction of fetal red blood cells leads to anemia, jaundice, heart failure, and severe complications if left untreated.
Understanding erythroblastosis fetalis is crucial for medical professionals, expecting mothers, and caregivers. With proper screening, diagnosis, and preventive care, this condition can often be avoided or successfully managed.
What is Erythroblastosis Fetalis?
Erythroblastosis fetalis is an immune-mediated hemolytic disease of the fetus and newborn. It occurs when the Rh-negative mother’s antibodies cross the placenta and attack the Rh-positive red blood cells of the fetus. The resulting hemolysis leads to severe anemia, and the fetus compensates by producing immature red blood cells called erythroblasts, hence the name erythroblastosis.
This disorder may also occur due to ABO incompatibility, though such cases are usually less severe compared to Rh incompatibility
Causes of Erythroblastosis Fetalis
The primary causes of erythroblastosis fetalis include:
1. Rh Incompatibility
The most common cause.
Occurs when:
• Mother is Rh-negative (lacking Rh antigen).
• Father is Rh-positive.
• Fetus inherits the Rh-positive blood group.
• During pregnancy or delivery, fetal red blood cells leak into the mother’s circulation, triggering the mother’s immune system to produce anti-Rh antibodies.
• In subsequent pregnancies, these antibodies cross the placenta and attack the fetal red blood cells.
2. ABO Incompatibility
Less common and usually less severe.
Occurs when:
• Mother has blood group O.
• Baby inherits A or B blood group.
• Mother’s naturally occurring anti-A or anti-B antibodies may cross the placenta and damage fetal red blood cells.
3. Other Blood Group Incompatibilities
Rarely, incompatibility with other minor blood group antigens such as Kell, Duffy, or Kidd can cause erythroblastosis fetalis.
4. Sensitizing Events
The risk of maternal sensitization increases due to:
• Previous blood transfusions with mismatched blood.
• Miscarriage or abortion without Rh prophylaxis.
• Ectopic pregnancy.
• Trauma during pregnancy.
Medical procedures like amniocentesis or chorionic villus sampling.
Pathophysiology
• Fetal red blood cells carrying Rh antigen enter maternal circulation.
• Mother’s immune system recognizes them as foreign and produces IgG antibodies.
• These antibodies cross the placenta in subsequent pregnancies.
• Antibodies attach to fetal red blood cells, causing hemolysis (destruction).
• Fetal bone marrow releases immature red cells (erythroblasts).
• Severe hemolysis results in anemia, hepatosplenomegaly, jaundice, hydrops fetalis, or even intrauterine death.
Signs and Symptoms of Erythroblastosis Fetalis
The severity of symptoms varies depending on the degree of hemolysis.
Prenatal (Before Birth) Signs
• Hydrops fetalis (generalized edema and fluid accumulation).
• Enlarged liver and spleen (hepatosplenomegaly).
• Severe anemia.
• Heart failure in the fetus.
• Excess amniotic fluid (polyhydramnios).
At Birth (Newborn Symptoms)
• Severe anemia (pale skin, lethargy).
• Jaundice (yellowing of skin and eyes due to high bilirubin).
• Enlarged liver and spleen.
• Difficulty breathing (respiratory distress).
• Swelling of the whole body.
• Poor feeding and irritability.
• In severe cases: stillbirth or neonatal death.
Complications
• If untreated, complications may include:
• Kernicterus (brain damage due to bilirubin deposition).
• Developmental delays.
• Neurological damage.
• Death in utero or shortly after birth.
Diagnosis of Erythroblastosis Fetalis
1. Maternal Screening
• Blood Group and Rh Typing: Done in early pregnancy.
• Indirect Coombs Test (ICT): Detects maternal antibodies against Rh antigen.
2. Fetal Diagnosis
• Ultrasound: Detects hydrops fetalis, hepatosplenomegaly, or ascites.
• Middle Cerebral Artery Doppler: Measures blood flow to detect fetal anemia.
• Amniocentesis: Checks bilirubin levels in amniotic fluid (Liley’s chart).
• Cordocentesis (PUBS): Direct sampling of fetal blood to assess anemia.
3. Postnatal Diagnosis
• Direct Coombs Test (DCT): Detects antibodies attached to newborn’s red blood cells.
• Hemoglobin levels: To check severity of anemia.
• Serum bilirubin levels: To monitor risk of jaundice and kernicterus.
• Peripheral blood smear: Shows nucleated red blood cells (erythroblasts).
Prevention of Erythroblastosis Fetalis
Prevention plays a key role in reducing the risk of this life-threatening condition.
1. Rh Immunoglobulin (RhIg / Rho(D) Immune Globulin)
• Administered to Rh-negative mothers.
• Prevents maternal sensitization by destroying fetal Rh-positive cells before the mother’s immune system reacts.
Doses:
• At 28 weeks of pregnancy.
• Within 72 hours after delivery of Rh-positive baby.
• After any sensitizing event (miscarriage, abortion, ectopic pregnancy, trauma, or invasive procedures).
2. Proper Antenatal Care
• Early screening for blood group and Rh type.
• Regular monitoring for Rh-negative mothers.
• Avoid unnecessary transfusions or ensure Rh compatibility.
3. Family Planning
Informing Rh-negative women about the importance of prophylaxis in every pregnancy.
Treatment of Erythroblastosis Fetalis
Treatment depends on the severity of the condition.
1. Intrauterine Treatment
• Intrauterine Blood Transfusion (IUT):
• Performed through umbilical vein (PUBS).
• Provides compatible red blood cells to the fetus.
• Lifesaving in severe anemia.
Early Delivery:
If the fetus is mature enough, early induction may be considered.
2. Postnatal Treatment
Phototherapy:
• Converts bilirubin into water-soluble form for excretion.
• Effective in treating neonatal jaundice.
Exchange Transfusion:
• Removes sensitized red blood cells and excess bilirubin.
• Replaces with donor blood.
• Used in severe cases.
Intravenous Immunoglobulin (IVIg):
Reduces hemolysis by blocking antibody-mediated destruction.
Supportive Care:
• Oxygen therapy for respiratory distress.
• Fluids and electrolytes to manage hydrops fetalis.
• Iron supplementation and folic acid after stabilization.
Prognosis
• With early detection and treatment, most babies survive and lead healthy lives.
• Severe untreated cases may result in stillbirth, neonatal death, or long-term neurological complications.
• Timely administration of Rh immunoglobulin has drastically reduced incidence worldwide.
Key Points for Competitive Exams
1. Erythroblastosis fetalis = Hemolytic Disease of Newborn (HDN).
2. Most common cause = Rh incompatibility.
3. Prevented by anti-D immunoglobulin given to Rh-negative mothers.
4. Diagnostic test for mother = Indirect Coombs Test.
5. Diagnostic test for newborn = Direct Coombs Test.
6. Treatment includes intrauterine transfusion, phototherapy, and exchange transfusion.
Frequently Asked Questions (FAQs)
Q1. What is erythroblastosis fetalis?
It is a hemolytic disease of the newborn caused by maternal antibodies destroying fetal red blood cells, usually due to Rh incompatibility.
Q2. Can erythroblastosis fetalis be prevented?
Yes, by giving Rh immunoglobulin injections to Rh-negative mothers during and after pregnancy.
Q3. What are the symptoms in newborns?
Severe jaundice, anemia, swollen body, difficulty breathing, enlarged liver/spleen, and in extreme cases, stillbirth.
Q4. Which tests confirm the condition?
Indirect Coombs Test (mother), Direct Coombs Test (newborn), ultrasound, Doppler studies, and bilirubin tests.
Q5. What is the most effective treatment?
Treatment may include intrauterine transfusions, phototherapy, exchange transfusion, and supportive care.
Q6. Is ABO incompatibility dangerous?
It usually causes milder disease compared to Rh incompatibility but can still lead to jaundice in the newborn.
Conclusion
Erythroblastosis fetalis is a serious but preventable condition caused mainly by Rh incompatibility between the mother and fetus. With advancements in antenatal screening, Rh immunoglobulin prophylaxis, and modern treatment methods, the incidence and severity of this disorder have significantly reduced. Awareness among expecting mothers, early diagnosis, and timely intervention are the keys to preventing complications and ensuring a healthy future for both mother and child.
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Writer: Vandita Singh, Lucknow (GS India Nursing Group)