Chapter 50 Anemia
What Is Anemia?
Anemia is defined by a hemoglobin and/or hematocrit more than two standard deviations below the mean for age. Anemia is also classified according to red blood cell (RBC) size, as measured by mean corpuscular volume (MCV). Other RBC indices that may also be abnormal in anemia include mean corpuscular hemoglobin (MCH), a measure of the amount of hemoglobin in each RBC, and mean corpuscular hemoglobin concentration (MCHC), a measure of the concentration of hemoglobin within each RBC. This chapter provides a general discussion of anemia. Chapter 63 discusses specific anemias.
How Do Hemoglobin and Red Blood Cell Size Change with Age?
The newborn’s hemoglobin varies with gestational age, timing of umbilical cord clamping, and clinical condition at the time of birth. Hemoglobin concentration is high at birth for a healthy term infant. It then decreases during the first 2 months, after which it slowly increases until adult levels are achieved during adolescence. RBCs also change in size with advancing age: At birth, RBCs are large, with MCV of 110 to 120 fl. MCV decreases over the first 6 months of life to 70 to 79 fl and then slowly rises to adult levels (80-95 fl) during late childhood and adolescence. Table 50-1 gives the age-associated ranges for expected hemoglobin and MCV. Values for MCH and MCHC are available in standard references.
Table 50-1 Age-Related Values for Hemoglobin and Mean Corpuscular Volume
Age | Hemoglobin (g/dl) (± 2 SD) | Mean Corpuscular Volume (fl) (± 2 SD) |
---|---|---|
Newborn (full term) | 16.5 (3) | 108 (10) |
1 mo | 13.9 (3.2) | 101 (10) |
2 mo | 11.2 (1.8) | 95 (11) |
6–24 mo | 12.0 (1.5) | 78 (8) |
2–6 yr | 12.5 (1.0) | 81 (6) |
6–12 yr | 13.5 (2.0) | 86 (9) |
12–18 yr male | 14.5 (1.5) | 88 (10) |
12–18 yr female | 14.0 (2.0) | 90 (12) |
Adapted from Brunetti M, Cohen J: Hematology. In Robertson J, Shilkofski N: The Harriet Lane Handbook, ed 17, Philadelphia, 2005, Mosby, p 337.
What Causes Anemia?
Anemia can be caused by RBC loss, destruction, or lack of production. The causes of anemia vary, based on the age of the child. Causes of anemia are discussed in the Evaluation section and listed in Tables 50-2 and 50-3.
Table 50-2 Anemia with Decreased Reticulocyte Index (RI < 2)
Decreased MCV | Normal MCV | Increased MCV |
---|---|---|
Iron deficiency | Chronic infection | Vitamin B12 deficiency |
Thalassemia | Recent blood loss | Folate deficiency |
Lead (> 50 μg/dl) | Marrow failure | Metabolic disease |
Copper deficiency | Malignancy | Chemotherapy |
Chronic infection | Aplastic anemia | EtOH |
Transient erythroblastopenia | Hypothyroidism | |
Diamond-Blackfan syndrome | Myelodysplasia | |
Renal failure (chronic) | Drugs |
EtOH, Ethanol; MCV, mean corpuscular volume.
EVALUATION
How Do I Assess Anemia in a Young Infant?
In the first 6 months after birth, consider the length of gestation because most neonatal iron stores are deposited in the last trimester of pregnancy. A premature infant has high risk for early development of anemia. Review the newborn and maternal records to identify possible incompatibility of the ABO or Rh blood groups that might have caused hemolysis. Neonatal jaundice may also suggest underlying hemolytic disease. A newborn who had a complex postnatal course and spent time in the neonatal intensive care unit may be anemic because of the large amounts of blood drawn. If the patient is a twin, in utero twin-to-twin transfusion may have caused anemia. Perinatal problems, such as placental abruption or placenta previa, lead to excessive blood loss from the mother and the newborn. Did the mother take prenatal vitamins or experience any infections during the pregnancy?
How Do I Evaluate an Anemic Older Infant or Child?
A careful history should search for fever, bruising, or bleeding that might indicate a malignancy, such as leukemia or neuroblastoma, or marrow dysfunction, such as aplastic anemia. Lymphadenopathy or hepatosplenomegaly might suggest an infiltrative process or perhaps certain types of storage disease. Recent infections such as Epstein-Barr virus or parvovirus could have suppressed RBC production. Has the child experienced episodes of pallor, unexplained episodes of pain (particularly in the hands and feet, as is seen in young children with sickling disorders), or episodic jaundice (which would support a hemolytic cause for anemia)? Has there been blood loss in the stool, urine, or sputum that might indicate particular areas to evaluate?
How Do I Detect Nutritional Anemia?
A careful assessment of the child’s diet is important in the evaluation of anemia. Iron deficiency is the most common nutritional anemia, so ask about sources of iron in the current diet (see Chapter 63). Also inquire about feeding during infancy: When was the child switched from breast-feeding or infant formula to cow milk, which is both a poor source of iron and a cause of gastrointestinal bleeding in infants younger than 12 months? Does the child drink goat milk, which is deficient in folic acid? Does the child take a strictly vegetarian diet, which is deficient in vitamin B12? Does the child currently take vitamins with or without iron? Does the child eat non-food items (pica), which suggests iron deficiency and increases the risk of lead intoxication?
Do Medications Ever Cause Anemia?
Inquire about all medications, whether prescribed, over-the-counter, alternative, or herbal. Cephalosporins, penicillins, and others can cause the development of antibodies to RBCs. Sulfonamides may suppress red and white blood cell production as well as induce hemolysis in children with glucose-6-phosphate dehydrogenase (G-6PD) deficiency. Anticonvulsants may be associated with a macrocytic anemia.
How Does Family History Help in the Evaluation?
A family history of anemia, jaundice, splenectomy for reasons other than trauma, or cholecystectomy in young relatives could indicate hemolysis or hemoglobinopathy. If the ethnic background of the family members is African, Asian, or Mediterranean, the child’s anemia might be related to sickle cell diseases, G-6PD deficiency, thalassemia, or hemoglobin E.

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