Anemia of Prematurity (AOP) is a common and expected condition affecting infants born before 37 weeks of gestation. It is a predictable consequence of early birth and the physiologic adjustments that occur in the first months of life. While a decline in red blood cell count is normal for all newborns, AOP is a more pronounced and accelerated form that often requires medical attention. Understanding its underlying causes is essential for effective management.
Defining Anemia of Prematurity
Anemia of Prematurity is characterized by a low concentration of hemoglobin or a reduced count of red blood cells (RBCs) in the premature infant’s circulation. RBCs are responsible for carrying oxygen. AOP is an exaggerated version of the “physiological anemia of infancy” seen in full-term babies, but it is more severe and symptomatic in premature infants, especially those with very low birth weight.
The decline in hemoglobin typically reaches its lowest point, or nadir, between three and twelve weeks after birth. In full-term infants, this nadir is usually well-tolerated and rarely falls below 10 grams per deciliter (g/dL). In contrast, very low birth weight infants may see levels drop to approximately 7 g/dL, leading to clinical signs of distress. This occurs because the immature bone marrow temporarily struggles to keep pace with the body’s rapidly changing demands.
Factors Unique to Prematurity Causing AOP
The primary mechanism driving AOP is the premature infant’s limited ability to produce new red blood cells efficiently. Fetal red blood cells have a naturally shorter lifespan, surviving only 40 to 60 days compared to 120 days for adult cells. As these cells break down, the body cannot keep up with replacement.
Insufficient production of erythropoietin (EPO) is another major contributor. EPO is the hormone that signals the bone marrow to produce red blood cells. After birth, the sudden increase in oxygen suppresses EPO production compared to the womb environment. For premature infants, this suppression is pronounced, and their immature kidneys are less responsive to the low oxygen state that normally triggers EPO release.
Rapid somatic growth also contributes by increasing the infant’s total blood volume faster than new cells can be generated, diluting the existing red cell mass. Furthermore, frequent diagnostic blood sampling required by intensive care causes iatrogenic blood loss, worsening the anemia. Lastly, premature infants have lower iron stores because the bulk of iron transfer from the mother occurs late in the third trimester.
Recognizing the Signs and Diagnosis
Recognizing Anemia of Prematurity can be challenging because its symptoms are often subtle and masked by other complications of prematurity. Clinicians look for specific observable signs that signal the condition is becoming symptomatic, such as pallor (noticeable paleness of the skin) and lethargy.
Other indicators relate to the infant’s cardiopulmonary status, as the body struggles to deliver sufficient oxygen. Symptoms may include increased heart rate (tachycardia), rapid breathing (tachypnea), or episodes of apnea and bradycardia. Poor feeding, diminished activity, and failure to gain weight are also common signs accompanying significant anemia.
AOP is confirmed through laboratory testing, specifically a Complete Blood Count (CBC). This test measures the concentration of hemoglobin and the percentage of red blood cells (hematocrit). A reticulocyte count is also used to assess how vigorously the bone marrow is responding. A combination of clinical symptoms and low lab values guides the medical team’s decision-making.
Treatment and Management Strategies
The management of Anemia of Prematurity involves minimizing blood loss and supporting the body’s red blood cell production. A primary strategy in the NICU is implementing blood conservation techniques. This involves using micro-sampling devices and strict protocols to reduce the volume and frequency of blood drawn for laboratory testing, which contributes significantly to anemia.
Iron supplementation is necessary to support the production of new red blood cells. Premature infants require supplemental iron, typically given orally, to provide the raw material for hemoglobin synthesis. Iron is often started early, around two weeks of age, ensuring the body has the necessary stores for robust red cell production.
For significant anemia, physicians may use Erythropoietin (EPO), an erythropoiesis-stimulating agent. Synthetic EPO stimulates the immature bone marrow to increase red blood cell production. While EPO does not eliminate the need for transfusions, it can modestly reduce the number of late red blood cell transfusions an infant receives.
Red blood cell transfusion remains the primary treatment for symptomatic or severe anemia, especially in the smallest infants. The decision to transfuse packed red blood cells is based on the infant’s hemoglobin levels and clinical condition, such as the need for respiratory support or the presence of apnea. Transfusions are typically given in small volumes to avoid fluid overload.
Current practice favors a restrictive transfusion strategy, meaning transfusions are given only when the infant is symptomatic or when hemoglobin drops below a specific, lower threshold. This approach, which has been shown to be as safe as a more liberal approach, minimizes the number of transfusions and associated risks, such as exposure to multiple donors. Over 80% of extremely low birth weight infants receive at least one red blood cell transfusion during their hospital stay.