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ANEMIA OF
PREMATURITY
DR.ODONG RICHARD JUSTIN.
PAEDIATRICIAN.
FORTPORTAL REGIONAL
REFERRAL HOSPITAL.
INTRODUCTION.
• Erythropoiesis decreases after
birth.
• Because of increased tissue
oxygenation.
• In term infants, the hemoglobin
level typically reaches an average
nadir of 11 g/dL at approximately
8 to 12 weeks after birth.
PATHOGENESIS.
• Primary cause of anemia of
prematurity (AOP) is the impaired
ability to increase serum
erythropoietin (EPO).
• 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.
Other factors for AOP.
• Blood loss from phlebotomy.
• Reduced red blood cell life span.
• Iron depletion.
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.
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.
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.
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.
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.
MANAGEMENT.
• Optimal nutrition (Iron
supplementation).
• Red blood cell transfusions are
primarily.
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.
Transfusion.
• RBC transfusion is the most
rapidly effective treatment for
AOP.
• Transfusion is a temporary
measure.
• Performed when the level of
anemia becomes symptomatic.
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.
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.
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.
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.
• 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.
• Administration of recombinant
human erythropoietin (EPO)
appears to have limited efficacy.
• We recommend NOT to routinely
administer EPO to preterm
infants.
THANKS.

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Anemia of prematurity

  • 1. ANEMIA OF PREMATURITY DR.ODONG RICHARD JUSTIN. PAEDIATRICIAN. FORTPORTAL REGIONAL REFERRAL HOSPITAL.
  • 2. INTRODUCTION. • Erythropoiesis decreases after birth. • Because of increased tissue oxygenation.
  • 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.
  • 12. MANAGEMENT. • Optimal nutrition (Iron supplementation). • Red blood cell transfusions are primarily.
  • 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.