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Anemia of Prematurity

Anemia of Prematurity: Pathogenesis and clinical findings Premature infants grow rapidly after birth to compensate for shortened gestation Neonatal erythropoietin (EPO) is produced in liver (rather than kidneys after neonatal period) Premature birth shortens 3rd trimester duration ↑ Red blood cell (RBC) demand consumes available iron Blood volume rapidly ↑ ↑ Risk of complications in preterm infants Immature liver has ↓ response to hypoxia ↓ Placental iron transfer to fetus ↓ Available iron stores Repeated blood draws for monitoring ↓ Plasma EPO ↓ RBC production Hemodilution ↑ Relative blood loss Anemia of Prematurity Hemoglobin nadir (lowest point) of 70-80g/L in preterm infants <32 weeks gestation at 4-6 weeks of age ↓ Hgb available for O2 transport to tissues Compensatory mechanisms triggered in response to ↓ tissue perfusion ↓ Cerebral perfusion ↓ Function of intestinal mucosa ↓ Metabolic rate ↑ Cardiac output to ↑ O2 delivery Immature respiratory centers in brainstem have paradoxical response to hypoxia ↓ Iron delivery to cerebrum ↓ Nutrient absorption ↑ Fatigue & ↓ endurance ↓ Neuronal metabolism, neurotransmitter production & myelination Poor growth ↓ Nutrient consumption Poor feeding Lethargy Tachycardia Apnea of prematurity** Impaired neurodevelopment Legend: Authors: Katelyn du Plessis Reviewers: Taylor Krawec Emily J. Doucette Lindsay Stockdale* * MD at time of publication Immature RBCs are more susceptible to oxidative injury ↑ Proportion of fetal hemoglobin (Hgb) compared to term infant ↓ RBC life span ↑ RBC destruction Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications ↓ Circulating RBCs Pallor Destroyed RBCs release Hgb into bloodstream Liver converts heme into bilirubin ↑ Unconjugated bilirubin Physiologic neonatal jaundice** **See corresponding Calgary Guide slide Published Aug 28, 2025 on www.thecalgaryguide.com