Anemia
Helen A. Christou
I. HEMATOLOGIC PHYSIOLOGY OF THE NEWBORN
(1, 2, 3, 4, 5). Significant changes occur in the red blood cell (RBC) mass of an infant during the neonatal period and ensuing months. The evaluation of anemia must take into account this developmental process, as well as the infant’s physiologic needs.
Normal development: The physiologic anemia of infancy (1)
In utero, the fetal aortic oxygen saturation is 45%, the erythropoietin levels are high, and the RBC production is rapid. The fetal liver is the major site of erythropoietin production.
After birth, the oxygen saturation is 95%, and the erythropoietin is undetectable. RBC production by day 7 is < 1/10th the level in utero. Reticulocyte counts are low, and the hemoglobin level falls (see Table 45.1).
Despite dropping hemoglobin levels, the ratio of hemoglobin A to hemoglobin F increases and the levels of 2,3-diphosphoglycerate (2, 2,3-DPG) (which interacts with hemoglobin A to decrease its affinity for oxygen, thereby enhancing oxygen release to the tissues) are high. As a result, oxygen delivery to the tissues actually increases. This physiologic “anemia” is not a functional anemia in that oxygen delivery to the tissues is adequate. Iron from degraded RBCs is stored.
At 8 to 12 weeks, hemoglobin levels reach their nadir (see Table 45.2), oxygen delivery to the tissues is impaired, renal erythropoietin production is stimulated, and RBC production increases.
Infants who have received transfusions in the neonatal period have lower nadirs than normal because of their higher percentage of hemoglobin A (1).
During this period of active erythropoiesis, iron stores are rapidly utilized. The reticuloendothelial system has adequate iron for 15 to 20 weeks in term infants. After this time, the hemoglobin level decreases if iron is not supplied.
RBC mass and iron stores are decreased because of low birth weight; however, hemoglobin concentrations are similar in preterm and term infants.
The hemoglobin nadir is reached earlier than in the term infant because of the following:
RBC survival is decreased in comparison with the term infant.
There is a relatively more rapid rate of growth in premature babies than in term infants. For example, a premature infant gaining 150 g/week requires approximately a 12 mL/week increase in total blood volume.
Table 45.1 Hemoglobin Changes in Babies in the First Year of Life
Week
Hemoglobin level
Term babies
Premature babies (1, 1,200-2,500 g, 500 g)
Small premature babies (<1,200 g)
0
17.0
16.4
16.0
1
18.8
16.0
14.8
3
15.9
13.5
13.4
6
12.7
10.7
9.7
10
11.4
9.8
8.5
20
12.0
10.4
9.0
50
12.0
11.5
11.0
Source: Glader B, Naiman JL. Erythrocyte disorders in infancy. In: Taeusch HW, Ballard RA, Avery ME, eds. Diseases of the Newborn. Philadelphia: WB Saunders; 1991.
Many preterm infants have reduced red cell mass and iron stores because of iatrogenic phlebotomy for laboratory tests. This has been somewhat ameliorated with the use of microtechniques.
Vitamin E deficiency is common in small premature infants, unless the vitamin is supplied exogenously.
The hemoglobin nadir in premature babies is lower than in term infants, because erythropoietin is produced by the term infant at a hemoglobin level of 10 to 11 g/dL and is produced by the premature infant at a hemoglobin level of 7 to 9 g/dL.
Iron administration before the age of 10 to 14 weeks does not increase the nadir of the hemoglobin level or diminish its rate of reduction. However, this iron is stored for later use.
Once the nadir is reached, RBC production is stimulated, and iron stores are rapidly depleted because less iron is stored in the premature infant than in the term infant.
Table 45.2 Hemoglobin Nadir in Babies in the First Year of Life | |||||||||||||||
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II. ETIOLOGY OF ANEMIA IN THE NEONATE (6)
Blood loss is manifested by a decreased or normal hematocrit (Hct), increased or normal reticulocyte count, and a normal bilirubin level (unless the hemorrhage is retained) (4, 5). If blood loss is recent (e.g., at delivery), the Hct and reticulocyte count may be normal, and the infant may be in shock. The Hct will fall later because of hemodilution. If the bleeding is chronic, the Hct will be low, the reticulocyte count will go up, and the baby will be normovolemic.
Obstetric causes of blood loss, including the following malformations of placenta and cord:
Abruptio placentae
Placenta previa
Incision of placenta at cesarean section
Rupture of anomalous vessels (e.g., vasa previa, velamentous insertion of cord, or rupture of communicating vessels in a multilobed placenta)
Hematoma of cord caused by varices or aneurysm
Rupture of cord (more common in short cords and in dysmature cords)
Occult blood loss
Fetomaternal bleeding may be chronic or acute. It occurs in 8% of all pregnancies; and in 1% of pregnancies, the volume may be as large as 40 mL. The diagnosis of this problem is by Kleihauer-Betke stain of maternal smear for fetal cells (2). Chronic fetal-to-maternal transfusion is suggested by a reticulocyte count >10%. Many conditions may predispose to this type of bleeding:
Placental malformations—chorioangioma or choriocarcinoma
Obstetric procedures—traumatic amniocentesis, external cephalic version, internal cephalic version, breech delivery
Spontaneous fetomaternal bleeding
Fetoplacental bleeding
Chorioangioma or choriocarcinoma with placental hematoma
Cesarean section, with infant held above the placenta
Tight nuchal cord or occult cord prolapse
Twin-to-twin transfusion
Bleeding in the neonatal period may be due to the following causes:
Intracranial bleeding associated with:
Prematurity
Second twin
Breech delivery
Rapid delivery
Hypoxia
Massive cephalhematoma, subgaleal hemorrhage, or hemorrhagic caput succedaneum
Retroperitoneal bleeding
Ruptured liver or spleen
Adrenal or renal hemorrhage
Gastrointestinal bleeding (maternal blood swallowed from delivery or breast should be ruled out by the Apt test) (see Chap. 43):
Peptic ulcer
Necrotizing enterocolitis
Nasogastric catheter
Bleeding from umbilicus
Iatrogenic causes. Excessive blood loss may result from blood sampling with inadequate replacement.
Hemolysis is manifested by a decreased Hct, increased reticulocyte count, and an increased bilirubin level (1, 2).
Immune hemolysis (see Chap. 26)
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