(USMLE topics) Pathophysiology of HDN, Signs and Symptoms, Prevention and Treatment options.

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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.