3. INTRODUCTION
• Physiological adaptation to extrauterine life
• Characterized by progressive decline in Hb
level within 1st week of life
• Persists for 6-8 weeks
• Hb level reaches 11g/dl (rarely falls below
10g/dl)
4. Pathophysiology
With the onset of respiration, more O2 becomes available for binding
to Hb
Hb-O2 saturation increases from 50%to 95% or more
Normal developmental switch from HbF to HbA
Increase in Blood O2 content and delivery
Downregulation of EPO production and suppression of Erythropoiesis
RBC removed from circulation not replaced
Hb level decreases
5. When will erythropoiesis resume?
• Hb concentration continues to decline until O2
needs become greater than O2 delivery
• Normally reached between 8-12 weeks of age
• EPO production increases and erythropoiesis
resumes
6.
7. Iron levels
• The supply of stored reticuloendothelial Iron,
derived from previous degraded RBC remains
sufficient for renewed Hb synthesis
• Even in absence of dietary Iron,until 20 weeks
of age
• No Iron supplements required before 4
months of life
8. Treatment
In full term infants:
• Ensuring that the diet contains essential
nutrients for hematopoiesis
• No other treatment required
9. Physiological anemia of Prematurity
• Exaggerated physiological Hb decline
• Hb decline more extreme and rapid
• 7-9g/dl reached by 3-6 weeks
Causes:
• Blood loss from repeated phlebotomies
• Shortened life span of RBC (40-60 days)
• Rapid growth
• Lower plasma EPO levels for the degree of
anemia
10. During fetal life, EPO produced by liver
Liver’s O2 sensor relatively insensitive to hypoxia
compared to kidney
Preterm babies rely primarily on liver for EPO
synthesis
Diminished responsiveness to anemia
Decline in Hb
12. Treatment
Dictated by infant’s clinical condition:
• Reducing unnecessary blood draws
• Transfusion when symptomatic
• Recombinant human EPO
• Iron therapy (1-2mg/kg/day of elemental Iron)