Diagnostic approach to anemia in newborn infants
Diagnostic approach to anemia in newborn infants
Anemia in the Newborn Infant
Hemoglobin increases with advancing gestational age: at term, cord blood hemoglobin is 16.8 g/dL (14–20 g/dL); hemoglobin levels in very low birthweight (VLBW) infants are 1–2 g/dL below those at term ( Fig. 103-1 ). Less than the normal range of hemoglobin for birthweight and postnatal age is defined as anemia. A “physiologic” decrease in hemoglobin content is noticed at 8–12 wk in term infants (hemoglobin, 11 g/dL) and at about 6 wk in premature infants (7–10 g/dL).
Infants born by cesarean section may have a lower hematocrit (Hct) than do those born vaginally. Anemia at birth is manifested as pallor, heart failure, or shock ( Fig. 103-2 ). It may be due to acute or chronic fetal blood loss, hemolysis, or underproduction of erythrocytes. Specific causes include hemolytic disease of the newborn, tearing or cutting of the umbilical cord during delivery, abnormal cord insertion, communicating placental vessels, placenta previa or abruptio, nuchal cord, incision into the placenta, internal hemorrhage (liver, spleen, intracranial), α-thalassemia, congenital parvovirus infection or other hypoplastic anemias, and twin-twin transfusion in monozygotic twins with arteriovenous placental connections.
Transplacental hemorrhage with bleeding from the fetal into the maternal circulation has been reported in 5–15% of pregnancies, but, unless severe, it is not usually sufficient to cause clinically apparent anemia at birth. The cause of transplacental hemorrhage is not clear, but its occurrence has been proven by demonstrating significant amounts of fetal hemoglobin and red blood cells (RBCs) in maternal blood on the day of delivery by the Kleihauer-Betke test or by flow cytometry methods to detect fetal cells in maternal blood. If the infant has severe anemia with heart failure, emergency exchange transfusion to restore Hct and oxygen-carrying capacity may be needed.
Acute blood loss usually results in severe distress at birth, initially with a normal hemoglobin level, no hepatosplenomegaly, and early onset of shock. In contrast, chronic blood loss in utero produces marked pallor, less distress, a low hemoglobin level with microcytic indices, and, if severe, heart failure.
Anemia appearing in the first few days after birth is also most frequently a result of hemolytic disease of the newborn. Other causes are hemorrhagic disease of the newborn, bleeding from an improperly tied or clamped umbilical cord, large cephalohematoma, intracranial hemorrhage, or subcapsular bleeding from rupture of the liver, spleen, adrenals, or kidneys. Rapid decreases in hemoglobin or Hct values during the first few days of life may be the initial clue to these conditions.
Later in the neonatal period, delayed anemia may develop as a result of hemolytic disease of the newborn, with or without exchange transfusion or phototherapy. Congenital hemolytic anemia (spherocytosis) occasionally appears during the 1st mo of life, and hereditary nonspherocytic hemolytic anemia has been described during the neonatal period secondary to deficiency of glucose-6-phosphate dehydrogenase (G6PD) and pyruvate kinase. Bleeding from hemangiomas of the upper gastrointestinal tract or from ulcers caused by aberrant gastric mucosa in a Meckel diverticulum or duplication is a rare source of anemia in newborns. Repeated blood sampling of infants requiring frequent monitoring of blood gas and chemistry parameters is a common cause of anemia among hospitalized infants. Deficiency of minerals such as copper may cause anemia in infants maintained on total parenteral nutrition.
Anemia of prematurity occurs in low birthweight infants 1–3 mo after birth, is associated with hemoglobin levels below 7–10 g/dL, and is clinically manifested as pallor, poor weight gain, decreased activity, tachypnea, tachycardia, and feeding problems. Repeated phlebotomy for blood tests, shortened RBC survival, rapid growth, and the physiologic effects of the transition from fetal (low Pao2 and hemoglobin saturation) to neonatal life (high Pao2 and hemoglobin saturation) contribute to anemia of prematurity. The oxygen available to neonatal tissue is lower than that in adults, but a neonate's erythropoietin response is attenuated for the degree of anemia and, as a result, hemoglobin and reticulocyte levels are low. In VLBW infants, delayed clamping of the umbilical cord with the infant held below the level of the placenta may enhance placental-infant transfusion and reduce postnatal transfusion needs. This maneuver should not delay any needed resuscitation and may lead to hyperviscosity.
Treatment of neonatal anemia by blood transfusion depends on the severity of symptoms, the hemoglobin level, and the presence of co-morbid diseases (bronchopulmonary dysplasia, cyanotic congenital heart disease, respiratory distress syndrome) that interfere with oxygen delivery. The need for treatment with blood should be balanced against the risks of transfusion, including hemolytic transfusion reactions, exposure to blood product preservatives and other potential toxins, volume overload, possible increased risk of retinopathy of prematurity and necrotizing enterocolitis, graft vs host reaction, and transfusion-acquired infection (cytomegalovirus [CMV], HIV, parvovirus, hepatitis B and C) (see Chapter 474 ). The risk of CMV infection can be almost eliminated by the use of leukoreduced blood. In the infant under 1,500 g, CMV antibody-negative leukoreduced blood should be used. The risk of acquiring HIV and hepatitis B and C viruses is reduced but not eliminated by antibody screening of donated blood. Blood banking techniques that limit multiple donor exposure should be encouraged. Although transfusion guidelines for preterm infants have been proposed, they have not been subjected to rigorous clinical study. Nonetheless, these guidelines have led to a decline in the number of unnecessary transfusions.
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