Hemolytic Disease of the Newborn, Animation


Hemolytic disease of the newborn, HDN, is
a condition in which red blood cells of a newborn infant, or a perinatal fetus, are
destroyed prematurely, resulting in anemia. HDN occurs when the blood types of the mother
and baby are incompatible. A blood type refers to the presence or absence
of a certain antigen, on the surface of a person’s red blood cells. Incompatibility happens when the baby has
an antigen that the mother does not have. The mother’s immune system interprets the
antigen as “foreign” and produces antibodies to target the cells carrying it for destruction. While in principle HDN may occur with mismatch
in any blood group, severe cases most commonly involve D-antigen of the Rh system. Specifically, HDN may develop if an Rh-negative
mother, having no D-antigen, carries an Rh-positive fetus, with D-antigen. The first mismatch pregnancy, however, is
usually not at risk. This is because the placenta normally does
a good job separating the mother’s blood from the fetal blood, preventing the fetal
red blood cells from being exposed to the mother’s immune system. However, at birth, or if a miscarriage or
abortion occurs, the tearing of the placenta exposes fetal blood to the mother, who then
responds by producing anti-D antibodies. Because antibody production takes some time,
it does not affect the first baby; but if the mother is again pregnant with another
Rh-positive fetus, her antibodies, being small enough to cross the placenta, can now cause
hemolysis. The first mismatch pregnancy may be at risk
if the mother has previously been exposed to the antigen in other ways, such as through
blood transfusion or sharing needles, or if the placental barrier is breached because
of trauma, or medical procedures early in the pregnancy. Anemia can cause heart failure, respiratory
distress, and edema. Infants born with HDN also develop jaundice
due to the accumulation of bilirubin, a yellow product of hemoglobin breakdown. Because red blood cells are destroyed rapidly
and infants are unable to excrete bilirubin effectively, its levels rise quickly within
24h of birth. Bilirubin is toxic for brain tissues and may
cause irreversible brain damage in a condition known as kernicterus. Other signs of HDN include enlarged liver,
spleen, and presence of immature red blood cells, erythroblasts, in the blood. Some of these signs can be detected before
birth, with ultrasound imaging. HDN that involves D-antigen can now be effectively
prevented with anti-D antibody. It is given to Rh-negative mothers during
and soon after the first mismatch pregnancy. The antibody binds to fetal blood cells that
leak into the mother’s blood, either destroying them, or hiding them from the mother’s immune
system, thus preempting the mother’s immune response. Infants born with HDN are usually treated
with intravenous fluid, and phototherapy, a procedure in which a certain spectrum of
light is used to convert bilirubin to a form that is easier for the infant to excrete. Severe anemia may be treated with:
– blood transfusion, – intravenous immunoglobulin G therapy, which
works by blocking the destruction of antibody-coated red blood cells. – and exchange transfusion, where the baby’s
blood is essentially replaced with Rh-negative donor blood. This procedure is very effective at removing
bilirubin and reducing the destructive effect of the mother’s antibody, but may have adverse
effects.


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