Anemia of newborn

Physiologic Anemia of the Newborn
• At one week postnatal all RBC indices begin declining to a
minimum value reached at about 2 months of age.
– decreased RBC production
– plasma dilution associated with increasing blood volume
– shorter life span on neonatal RBCs (50-70 days)
– more fragile RBCs
– switch from HbF to HbA
• HbF decreases about 3% per week
• at 6 mo. HbF represents only 2% of total Hb
• switch to HbA provides for greater unloading of oxygen to tissues d/t
lower oxygen affinity of HbA relative to HbF.
– seldom produces symptoms
– not altered by nutritional supplements

Anemia at Birth
• Etiology: usually caused by congenital
hemolytic disease of the newborn.
• Other causes include:
– bleeding from umbilical cord
– internal hemorrhage

Anemia of Prematurity
• Occurs in low birth weight infants w/ poor
erythropoietin response
– Protein content of breast milk may not be sufficient for
hematopoiesis in the premature infant.
– Hb level rapidly declines after birth to a low of 7-10 g/dl at
6 weeks of age.
– Signs and Symptoms
• apnea
• poor weight gain
• pallor
• decreased activity
• tachycardia

Background
• Anemia of prematurity (AOP) is an exaggerated, pathologic
response of the preterm infant. AOP is a normocytic,
normochromic anemia characterized by low serum EPO levels.
• 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.
• The risk of anemia of prematurity (AOP) is inversely related to
gestational maturity and birthweight. As many as half of
infants of less than 32 weeks gestation develop AOP.

Etiology
• Three basic mechanisms for the development
of anemia of prematurity (AOP) include:
– inadequate RBC production
– shortened RBC life span
– blood loss.

Presentation
• Many clinical findings have been attributed to anemia of
prematurity (AOP), but they are neither specific nor
diagnostic. These symptoms may include the following:
– Poor weight gain despite adequate caloric intake
– Cardiorespiratory symptoms such as tachycardia, tachypnea, and flow
murmurs
– Decreased activity, lethargy, and difficulty with oral feeding
– Pallor
– Increase in apneic and bradycardic episodes, and worsened periodic
breathing
– Metabolic acidemia - Increased lactic acid secondary to increased
cellular anaerobic metabolism in relatively hypoxic tissues

Treatment
Medical treatment options:
• Blood transfusion(s)
• Recombinant erythropoietin (EPO)
• Observation.

Observation
• Observation may be the best course of action for
infants who are asymptomatic, not acutely ill, and
are receiving adequate nutrition.
• Adequate amounts of vitamin E, vitamin B-12, folate,
and iron are important to blunt the expected decline
in hemoglobin levels in the premature infant.
• Periodic measurements of the hematocrit level in
infants with AOP are necessary.

Non-transfusion Approaches
• Decrease lab draws
• Enteral iron

New Transfusion Guidelines
March 2010
Transfusion Threshold Clinical Situation
Hgb 10g/dL Critically ill neonate,
ventilated or significant
pressor support
Hgb 8g/dL Infant on stable respiratory
support (CPAP/stable vent,
HFHNC for CPAP effect, or
NC
Hgb ≤7g/dL Infant requiring no
support