3. • In term infants, the hemoglobin
level typically reaches an average
nadir of 11 g/dL at approximately
8 to 12 weeks after birth.
4. PATHOGENESIS.
• Primary cause of anemia of
prematurity (AOP) is the impaired
ability to increase serum
erythropoietin (EPO).
5. • EPO is produced by the fetal liver
and the cortical interstitial cells
of the kidney in response to
hypoxia.
• Liver is the principal site of EPO
production in the fetus.
6. Other factors for AOP.
• Blood loss from phlebotomy.
• Reduced red blood cell life span.
• Iron depletion.
7. Blood loss from phlebotomy.
• Iatrogenic blood loss due to
phlebotomy for blood tests.
• Laboratory studies contributed to
iatrogenic blood loss by 2 to
4 mL/kg per week.
8. Reduced red blood cell life
span.
• Term infants is approximately 60
to 80 days.
• Range of 45 to 50 days in
extremely low birth weight infants
(ELBW).
• Reduced red cell life span
contributes to the severity of
anemia.
9. Iron depletion.
• Iron depletion may impair
recovery from AOP.
• Because of their rapid growth
rate, premature infants have
increased utilization and
depletion of iron stores.
• Administration of iron does not
inhibit the fall in hemoglobin
concentration due to AOP.
10. CLINICAL AND
LABORATORY FEATURES.
• Typically occurs at 3 to 12 weeks
after birth.
• Onset of AOP is inversely
proportional to the gestational
age at birth.
• Anemia typically resolves by three
to six months of age.
11. Laboratory findings.
• Anemia.
• Normocytic and normochromic
red blood cells.
• Reticulocyte count is low, and red
blood cell precursors in the bone
marrow are decreased.
• Serum concentrations of EPO are
low.
13. Iron supplementation.
• Iron stores depleted by two to
three months of age.
• As a result, all preterm infants
should receive iron
supplementation of 2 to
4 mg/kg per day through the first
year of life.
14. Transfusion.
• RBC transfusion is the most
rapidly effective treatment for
AOP.
• Transfusion is a temporary
measure.
• Performed when the level of
anemia becomes symptomatic.
15. Erythropoietin.
• Pathogenetic importance of
impaired EPO production in AOP
provides the rationale for the
therapy with recombinant human
EPO.
• Approach has not been accepted
widely because it appears to have
limited efficacy in decreasing the
number of blood donors to which the
infant is exposed via transfusion.
16. Complications.
• Use of EPO in premature infants
appears to be safe.
• Complications include the following:
• Transient neutropenia that resolves
with cessation of therapy.
• Iron deficiency occurs if
supplementation is inadequate.
17. Dose.
• Administered intravenously
(200 U/kg per dose once daily) or
subcutaneously (400 U/kg per
dose, 3 times per week).
• Infants treated with EPO require
iron supplementation.
18. SUMMARY AND
RECOMMENDATIONS.
• Newborn infants have a fall in
hematocrit soon after birth due
primarily to impaired production of
erythropoietin.
• Preterm infants, the decline occurs
earlier, is more pronounced, and is
called anemia of prematurity (AOP).
• AOP typically occurs at 3 to 12
weeks.
19. • Laboratory findings characteristic
of AOP include normocytic and
normochromic red blood cells, low
reticulocyte count, and low
erythropoietin levels.
• AOP may require treatment with
RBCs transfusion.
• Transfusion is a temporary.
20. • Administration of recombinant
human erythropoietin (EPO)
appears to have limited efficacy.
• We recommend NOT to routinely
administer EPO to preterm
infants.