Anemia in the newborn infant may result from many pathophysiologic processes. Because of the complex interrelations involving both mother and fetus, there is a broader list of causes of anemia in the neonatal period than is found at any other time of life. Anemia may be a consequence of three fundamental mechanisms: (1) loss of RBCs (hemorrhage); (2) rapid destruction of RBCs (hemolysis); or (3) underproduction of RBCs. The purpose of this review is to describe the mechanisms, clinical and laboratory features, and management of posthemorrhagic anemia in the newborn.1,2 Hemolytic and aregenerative anemias will be mentioned only briefly as differential diagnostic considerations.


Although perinatal hemorrhage may occur in many ways, its causes can be conveniently divided into two general groups (Table 1). First: external hemorrhage, usually from the umbilical cord or placenta, in which an external bleeding site is obvious. Second: occult hemorrhage into closed compartments. In these cases bleeding is usually suspected because of clinical signs of blood loss such as pallor and shock.


During uncontrolled or "precipitous" deliveries, a normal umbilical cord may rupture close to its attachment to the fetus. Rupture may also occur when the cord is abnormally short or excessively stretched by wrapping around the fetal neck or body.

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