All infants experience a decrease in hemoglobin concentration after birth. The transition from a relatively hypoxic state in utero to a relatively hyperoxic state with increased tissue oxygenation after birth leads to a decline in erythropoietin (EPO) concentration. For the term infant, a physiologic and usually asymptomatic anemia is observed 8-12 weeks after birth.
Anemia of prematurity (AOP) is an exaggerated, pathologic response of the preterm infant to this transition. AOP is a normocytic, normochromic, hyporegenerative anemia characterized by a low serum EPO level, often despite a remarkably reduced hemoglobin concentration. Nutritional deficiencies of iron, vitamin E, vitamin B-12, and folate may exaggerate the degree of anemia, as may blood loss and/or a reduced red cell life span.
AOP spontaneously resolves in many premature infants within 3-6 months of birth. In others, however, medical intervention is required. Although the physiology and pathophysiology for AOP are well studied, controversy surrounds the timing, method, and effectiveness of therapeutic interventions for AOP. This article reviews the pathophysiology of AOP, the means of reducing its impact on premature infants, and its treatment through blood transfusion or recombinant EPO therapy.
It is important to discuss with parents the normal course of anemia, the criteria for and risks associated with transfusions, and the advantages and disadvantages of erythropoietin (EPO) administration.