Diseases & Conditions



Anemia is a disorder in which there are too few red blood cells in the blood.

Normally, the newborn's bone marrow does not produce new red blood cells between birth and 3 or 4 weeks of age. Anemia can occur when red blood cells are broken down too rapidly, too much blood is lost, or more than one of these processes occurs at the same time.

Any process that leads to red blood cell destruction, if sufficiently severe, results in anemia and high levels of bilirubin (hyperbilirubinemia). Hemolytic disease of the newborn may cause the newborn's red blood cells to be destroyed rapidly. The red blood cells may also be rapidly destroyed if the newborn has a hereditary abnormality of the red blood cells. An example is hereditary spherocytosis, in which the red blood cells appear small and spherical in shape when viewed under a microscope.

Infections acquired before birth, such as toxoplasmosis, rubella, cytomegalovirus, herpes simplex, or syphilis, may also rapidly destroy red blood cells, as can bacterial infections of the newborn acquired during or following birth.

Another cause of anemia is blood loss. Blood loss can occur in many ways, for example, if there is a large transfusion of the fetal blood across the placenta and into the mother's circulation (fetal-maternal transfusion) or if too much blood gets trapped in the placenta at delivery, when the umbilical cord is clamped. The placenta may separate from the uterine wall before delivery (placental abruption), leading to hemorrhage of the fetal blood. Rarely, anemia may result from a failure of the fetal bone marrow to produce red blood cells. One example of this is a genetic disorder called Fanconi's anemia. Another rare example is that due to exposure of the mother and fetus to certain drugs used during pregnancy.

Symptoms and Treatment

A newborn who has suddenly lost a large amount of blood during labor or delivery may appear pale and have a rapid heart rate and low blood pressure, along with rapid, shallow breathing. Milder anemia may result in lethargy, poor feeding, or no symptoms. When the anemia is a result of rapid breakdown of red blood cells, there is also increased production of bilirubin, and the newborn's skin and the whites of the eyes appear yellow (jaundice).

A newborn who has rapidly lost a large amount of blood, often during labor and delivery, is treated with intravenous fluids followed by a blood transfusion. Very severe anemia caused by hemolytic disease may also require a blood transfusion, but the anemia is more often treated with an exchange blood transfusion, in which part of the newborn's blood is gradually removed and replaced with equal volumes of fresh donor blood. The exchange transfusion also removes bilirubin in the circulation and thus treats the hyperbilirubinemia.

What Is Hemolytic Disease of the Newborn?

Hemolytic disease of the newborn (also called erythroblastosis fetalis) is a condition in which red blood cells are broken down or destroyed more rapidly than is normal. The newborn's red blood cells are destroyed by antibodies that were produced by the mother and crossed the placenta from the mother's circulation into the fetal circulation before delivery. A mother who is Rh-negative may have produced antibodies against Rh-positive blood cells after she was exposed to red blood cells of a previous fetus that was Rh-positive. Such exposure may occur during pregnancy or labor, but may also occur if the mother had been accidentally transfused with Rh-positive blood at any time earlier in life.

The mother's body responds to the “incompatible blood” by producing antibodies to destroy the “foreign” Rh-positive cells. These antibodies cross the placenta during a subsequent pregnancy. If the fetus she is carrying is Rh-negative, there is no consequence. However, if the fetus has Rh-positive red blood cells, the mother's antibodies attach to, and start to destroy, the fetal red blood cells, leading to anemia of varying degrees. This anemia begins in the fetus and continues after delivery.

Sometimes other blood group incompatibilities may lead to similar hemolytic diseases. For example, if the mother is blood type O and the fetus has blood type A or B, then the mother's body produces anti-A or anti-B antibodies that can cross the placenta, attach to fetal red blood cells, and lead to their breakdown (hemolysis). Rh incompatibility usually leads to more severe anemia than ABO incompatibility.

Prevention of hemolytic disease due to Rh incompatibility involves injecting the mother with a Rh 0 (D) immune globulin preparation at about 28 weeks of pregnancy and again immediately after delivery. Injection of this immune globulin rapidly destroys any Rh-positive fetal red blood cells that have entered the mother's circulation before they stimulate the mother's body to produce antibodies.

Severe anemia caused by hemolytic disease of the newborn is treated in the same way as any other anemia. The doctor also observes the newborn for jaundice, which is likely to occur because hemoglobin from the red blood cells that are being rapidly broken down is converted to the yellow pigment, bilirubin, giving the newborn's skin and whites of the eyes a yellow appearance. Jaundice can be treated by exposing the newborn to bright lights (phototherapy) or by having the newborn undergo an exchange blood transfusion. Very high levels of bilirubin in the blood can lead to brain damage (kernicterus).

Last full review/revision February 2003

Source: The Merck Manual Home Edition