PHYSIOLOGICAL ANEMIA OF INFANCY

Physiological anemia of infancy refers to postnatal drop in Hb levels among normal children due to developmental changes in rate of erythropoiesis and RBC destruction. In term infants, Hb levels fall gradually to reach their nadir (9-11 gm/dl) by 2-3 months, before rising again.

Etiopathogenesis: Normal newborns have higher Hb and Hct levels due to higher metabolic needs and lower oxygen tension in transplacental blood supply. Postnatally, these levels decline progressively due to many factors, including:

• Increased hemolysis due to shorter life-span of fetal RBCs as compared to adult RBCs.

• Decreased erythropoiesis due to:

- Increased O₂ tension after initiation of 'self-breathing' that inhibits erythropoietin activity;

- Increased release of O₂ from adult RBCs, which have lesser O₂ affinity than fetal RBCs.

- Shift of EPO production from liver to juxta­glomerular cells, which are relatively more sensitive to oxygen tension.

Clinically, physiological anemia in normal infants is usually mild and asymptomatic. Exaggerated physiological anemia is seen in: (a) preterms due to poor iron stores,

(b) top-fed children due to poor assimilation of dietary iron, and (c) babies with perinatal blood loss, e.g. fetofetal transfusion and Rh-hemolytic disease.

Treatment: No treatment is necessary in most cases, as erythropoiesis resumes to desired rate soon after the nadir is reached. Physiological anemia is unlikely to respond to iron or folic acid supplements due to low EPO levels and hence, some cases of exaggerated physiological anemia may require blood transfusion.

Recombinant EPO therapy has been tried in some cases with equivocal benefits and usually unnecessary. However, iron supplements should be started at 4-8 weeks in preterms and at 4 months in term infants to prevent iron deficiency anemia.

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