Anemia of prematurity

ANEMIA OF PREMATURITY IS A PROBLEM WORTH KNOWING IN ANY MEDICAL PRACTITIONER INVOLVED IN THE CARE OF PREMATURE INFANTS.

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. P rimary 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. L iver 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. I atrogenic blood loss due to phlebotomy for blood tests. L aboratory studies contributed to iatrogenic blood loss by 2 to 4 mL/kg per week.

8. Reduced red blood cell life span. T erm infants is approximately 60 to 80 days. R ange of 45 to 50 days in extremely low birth weight infants (ELBW ). R educed red cell life span contributes to the severity of anemia.

9. Iron depletion. I ron depletion may impair recovery from AOP. Because of their rapid growth rate, premature infants have increased utilization and depletion of iron stores. A dministration of iron does not inhibit the fall in hemoglobin concentration due to AOP.

10. CLINICAL AND LABORATORY FEATURES. T ypically occurs at 3 to 12 weeks after birth. O nset of AOP is inversely proportional to the gestational age at birth. A nemia typically resolves by three to six months of age.

11. Laboratory findings. Anemia. N ormocytic and normochromic red blood cells. R eticulocyte 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. I ron stores d epleted 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. T ransfusion is a temporary measure. Performed when the level of anemia becomes symptomatic.

15. Erythropoietin. P athogenetic importance of impaired EPO production in AOP provides the rationale for the therapy with recombinant human EPO. A pproach 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: T ransient neutropenia that resolves with cessation of therapy. Iron deficiency occurs if supplementation is inadequate.

17. Dose. A dministered 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. L aboratory 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. T ransfusion 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 .

21. THANKS.