• Overview

Erythroblastosis fetalis is a disease of the fetus and newborn child

characterized by agglutination and phagocytosis of the fetus’s red blood
cells.

- Mother- Rh-
Father- Rh+
Fetus- Rh+

- Fetus rbc diffuse through placenta into mother’s blood. During second
pregnancy, if second child is also opposite Rh, mother’s anti-Rh agglutinins
diffuse through placenta into fetus’s blood.

• Incidence of the Disease

• Effect of the Mother’s Antibodies on the Fetus

https://youtu.be/8shHxq4X_5o
- Mother’s antibodies diffuse through placental membrane into fetus’s
blood, causing agglutination of fetus’s blood, and then hemolysis.
- Haemoglobin is released into bloodstream, macrophages convert it to
bilirubin-Hyperbilirubinemia, jaundice
- Antibodies also attack other bodily cells.
• Clinical picture of Erythroblastosis
-Nucleated blastic forms are present- hence the name
- Jaundice, erythroblastosis, anemia-mother’s antibodies circulate for 1 or 2
months and kill more and more RBCs
- Hematopoietic tissue of liver and spleen tries to replace hemolyzed RBCs-
enlarged- produce RBCs like middle of gestation
- Anemia usually causes death
- Those who survive generally have kernicterus- high bilirubin content
damages nuronal cells-can’t reproduce

• Treatment of the Erythroblastotic Neonate

- Replacing neonate’s blood with Rh- blood
- Repeated several times during first few weeks, to keep bilirubin level low
and avoid kernictus
400 ml in 1.5 hrs while Rh+ blood is removed

• Prevention of Erythroblastosis Fetalis

- D antigen is responsible for immunization of mother’s blood.
- Rh immunoglobulin globulin- 28 to 30 weeks of gestation- Anti D antigen
- Rh immunoglobulin globulin- 28 to 30 weeks of gestation- Anti D antigen
- Inhibits antibody-induced B lymphocyte antibody production- shuts down
production of anti-Rh agglutinin in mother’s blood

• Transfusion Reactions
- Transfusion reactions are defined as adverse events associated with the
transfusion of whole blood or one of its components.

- Usually when such a reaction occurs, the donor’s blood gets agglutinated
rather than the recipient’s blood.
- Because the plasma from the donor’s blood gets diluted by plasma from
recipient’s blood, so titer of agglutinins in donor’s blood is less compared to
recipient’s blood, which causes agglutination of donor’s blood.
- The donor’s blood is lesser in quantity and thus cannot dilute the
recipient’s blood.

- All transfusion reactions result in:-

a) Immediate hemolysis- by hemolysins
OR
b) Delayed hemolysis- phagocytosis of agglutinated cells

- Hemoglobin-phagocytes-bilirubin-liver bile-intestines
 So person with normally functioning liver does not get jaundice unless 400+
ml of blood is hemolyzed in less than a day

• Acute Kidney Shutdown after transfusion reactions

-Begins in a few minutes or hours until death

- Renal vasoconstriction- due to toxins released by hemolyzed RBCs

- Circulatory shock- due to loss of circulatory red blood cells and said toxins,
arterial blood pressure drops, renal blood flow and urine output decreases.

- Renal Tubular Blockage- Excess hemoglobin unbinded with haptoglobins

enter kidneys and precipitates.
A small amount of hemoglobin can be absorbed by tubular epithelium of
the kidneys, but if there is a huge amount it settles down in solid form at the
bottom of kidney vessels, causing blockage.

-If shutdown is complete, patient will die within 7-12 days, unless treated
with an artificial kidney