Anemia developing during the neonatal period (0-28 days of life)
in infants of >34 weeks gestational age
central venous hemoglobin <13 g/dL or
a capillary hemoglobin <14.5 g/dL
< 8 weeks : Fetal Yolk Sac
8 weeks : Fetal Liver
24 weeks: Bone marrow
Stimulates proliferation of erythroid progenitors
Does not cross placenta
EPO concentration increases from 4 mU/ ml at 16 weeks gestation to 40 mU/ ml at 40 weeks
Gestational Age: Hb directly proportional to GA
18-20 w – 11.5 g/dL
23-25 w – 12.4 g/dL,
26-30 w – 13.4 g/dL,
32- 40w- 17.0 g/dL
Site of Sampling: capillary Hb > venous Hb
PHYSIOLOGIC ANEMIA OF INFANCY
In Utero: fetal oxygen saturation 45%
EPO levels increase RBC production, Retics 3-7%
Neonatal oxygen saturation increase 95%
EPO level decrease
RBC production decrease, Retics decrease 0 – 1% by day 7
8-12 Weeks :
Hb nadir in term infants – Hb drops to 10 g/ dl
EPO production increase, RBC production increase
Anemia in the newborn infant results from one of the three processes:
Loss of RBCs (Hemorrhagic anemia): most common
Increased destruction of RBCs (Hemolytic anemia)
Underproduction of RBCs (Hypoplastic anemia)
Loss of placental integrity : abruptio placentae, placenta previa, traumatic amniocentesis
Anomalies of the umbilical cord or placental vessel: velamentous insertion of the umbilical cord, vasa praevia, umbilical cord hematoma.
Twin-twin transfusion: the different in Hb concentration between twin is >5 g/dL
Traumatic rupture of the umbilical cord
Failure of placental transfusion: umbilical cord occlusion
Obstetric trauma: intracranial hemorrhage
Enclosed hemorrhage: caput succedaneum, cephalhematoma, intracranial hemorrhage
Defects in hemostasis: congenital coagulation factor deficiency, thrombocitopenia
Iatrogenic blood loss: loss of 20%
Isoimmune hemolytic anemia: Rh incompatibility
Autoimmune hemolytic anemia
Congenital erythrocyte defect
Metabolic enzyme deficiency: G6PD deficiency, pyruvate kinase deficiency
Membran defect: hereditary spherocytosis, hereditary elliptocytosis
Nutritional deficiency: Vit E deficiency
Congenital disease: Diamond-Blackfan syndrome, congenital leukemia
Acquired disease: infection, aplastic anemia.
Diamond- Blackfan syndrome – pure red cell aplasia
periodic breathing / apnea
increased work of breathing
lethargy, poor feeding
anerobic metabolism / lactic acidosis
Acute: pallor, tachypnea or gasping respirations, vascular instability.
Chronic: unexplained pallor, minimal sign of respiratory distress, liver enlargement.
Hemolytic anemia: jaundice, pallor, tachypnea, hepatosplenomegaly.
Hypoplastic anemia: presentation after 48 h age, absence of jaundice, reticulocytopenia.
History: obstetric, neonatal, family
Physical exam: signs of acute blood loss,hemolysis
Hb or Hct
Peripheral blood smear
Coomb’s test, Bilirubin level
Kleihauer – Betke
Kleihauer – Betke test
What is the cause of the anemia?
How well is the baby compensating?
How urgently does the anemia need to be corrected?
Risk / benefit analysis of treatment?
Simple replacement transfusion: acute hemorrhagic anemia
–type O, Rh-negative packed RBCs, fresh frozen plasma, dextran
Exchange transfusion: chronic hemolytic anemia, severe isoimmune hemolytic anemia.
Nutritional replacemen: iron, folate, vitamin E.
Packed Red Blood Cell Transfusions
Guidelines controversial and variable
Replace acute blood loss
Correct anemia that is compromising cardiovascular status or oxygen carrying capacity
Recombinant Human Erythropoietin
Reducing blood transfusions in anemia of prematurity
Over 20 controlled trials published
Modest benefit at best
Conservative transfusion criteria / ¯ phlebotomy loss
Cost effectiveness debated
Need for iron supplementation
Breast fed term babies: 0
Formula fed term babies:
iron fortified formula = 2 mg / kg/ day