Anemia is a disorder in which there are too few red blood cells in the blood. Normally, the bone marrow does not produce new red blood cells between birth and 3 or 4 weeks of age, causing a slow drop in the red blood cell count (called physiologic anemia) over the first 2 to 3 months of life. Very premature newborns have a slightly greater drop in red blood cell count. More severe anemia can occur when More than one of these processes can occur at the same time. Severe red blood cell breakdown results in anemia and high levels of bilirubin in the blood (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 look like small spheres when viewed under a microscope. Another rare example occurs in some infants who lack a specific red blood cell enzyme (glucose-6-phosphate dehydrogenase [G6PD]). In these infants, exposure of the mother and fetus to certain drugs used during pregnancy (such as aniline dyes, sulfa drugs, and many others) may result in rapid breakdown of red blood cells. Infections acquired before birth, such as toxoplasmosis, rubella, cytomegalovirus infection, herpes simplex virus infection, or syphilis, may also rapidly destroy red blood cells, as can bacterial infections of the newborn acquired during or after birth. Blood loss is another cause of anemia. Blood loss can occur in many ways. For example, blood is lost if there is a large transfusion of fetal blood across the placenta (the organ that connects the fetus to the uterus and provides nourishment to the fetus) and into the mother's circulation (fetal–maternal transfusion) or if too much blood gets trapped in the placenta at delivery, when the newborn is held above the mother's abdomen when the umbilical cord is clamped. Twin-to-twin transfusions, in which blood flows from one fetus to the other, can cause anemia in one twin and too much blood (polycythemia) in the other twin. The placenta may separate from the uterine wall before delivery (placental abruption), leading to hemorrhage of fetal blood. Rarely, failure of the fetal bone marrow to produce red blood cells may result in anemia. Examples of this lack of production include rare genetic disorders such as Fanconi's anemia and Diamond-Blackfan anemia. Some infections (such as cytomegalovirus infection, syphilis, and HIV) also prevent the bone marrow from producing red blood cells. Symptoms and Diagnosis Most infants with mild or moderate anemia have no symptoms. Moderate anemia may result in sluggishness (lethargy), poor feeding, or no symptoms. Newborns who have suddenly lost a large amount of blood during labor or delivery may be in shock and appear pale and have a rapid heart rate and low blood pressure, along with rapid, shallow breathing. When the anemia is a result of rapid breakdown of red blood cells, there is also an increased production of bilirubin, and the newborn's skin and whites of the eyes appear yellow (jaundice). Diagnosis is based on symptoms and is confirmed with blood tests. Treatment Most infants have mild anemia and do not require any treatment. Newborns who have rapidly lost large amounts of blood, often during labor and delivery, are 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, which lowers the bilirubin level as well as increases the red blood cell count. In an exchange transfusion, a small amount of the newborn's blood is gradually removed (one syringe at a time) and replaced with equal volumes of fresh donor blood. 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 normal, causing hyperbilirubinema, anemia, and in the most severe forms, death. Hemolytic disease of the newborn may occur in Rh-positive babies born to Rh-negative mothers. It develops when the newborn's red blood cells are destroyed by anti-Rh antibodies that were produced by the mother and passed through the placenta from the mother's circulation into the fetal circulation before delivery. A mother who is Rh-negative can produce antibodies against Rh-positive blood cells if she was previously exposed to red blood cells from a fetus that was Rh-positive. Such exposure may occur during pregnancy or labor, but it may also occur if the mother had been accidentally transfused with Rh-positive blood at any time earlier in life. The mother's body then 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. The rapid breakdown of red blood cells begins in the fetus and continues after delivery. Severe anemia caused by hemolytic disease of the newborn is treated in the same way as any other anemia. Doctors also observe 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), unless it is prevented by these measures. To prevent sensitization of Rh-negative women, the Rh antigen, an Rh0(D) immune globulin preparation, is given by injection at about 28 weeks of pregnancy and again immediately after delivery. Injection of this immune globulin prevents the mother's immune system from producing anti-Rh antibodies, and it also rapidly coats any Rh-positive fetal red blood cells that have entered the mother's circulation so they are not recognized as Rh-positive cells by the mother's immune system. This treatment usually prevents hemolytic disease of the newborn from developing. Sometimes other blood group incompatibilities may lead to similar (but milder) hemolytic diseases. For example, if the mother has 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 cause their breakdown (hemolysis), leading to mild anemia and hyperbilirubinemia. Rh incompatibility usually leads to more severe anemia than ABO incompatibility.
What Is Hemolytic Disease of the Newborn?
Saturday, April 3, 2010
Labels: Anemia in the Newborn
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