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neonatal anaemia.pdf

  1. Anemia of newborn
  2. 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
  3. Anemia at Birth • Etiology: usually caused by congenital hemolytic disease of the newborn. • Other causes include: – bleeding from umbilical cord – internal hemorrhage
  4. 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
  5. 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.
  6. Etiology • Three basic mechanisms for the development of anemia of prematurity (AOP) include: – inadequate RBC production – shortened RBC life span – blood loss.
  7. 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
  8. Treatment Medical treatment options: • Blood transfusion(s) • Recombinant erythropoietin (EPO) • Observation.
  9. 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.
  10. Non-transfusion Approaches • Decrease lab draws • Enteral iron
  11. 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