The tragedy of iron deficiency during infancy and early childhood☆☆☆★
Article Outline
See related article, p. 514 .
According to Webster’s New World Dictionary , a tragedy is a “very sad or tragic event or sequence of events.” Although some may not view iron deficiency in the early years of life as a tragedy, in many respects this disorder qualifies for such a designation. In this issue of The Journal, Kwiatkowski et al1 from the Children’s Hospital of Philadelphia remind us that severe iron deficiency remains a common problem, despite triumphal pronouncements and glowing commentaries during the past 10 to 15 years heralding its virtual disappearance in the United States.1, 2, 3 It is sad indeed that this easily preventable condition, characterized recently by a group of New York pediatricians as a “pediatric failure,”4 remains so prevalent in our country. If 55 cases of severe iron deficiency were seen during the past decade at one children’s hospital, how many equally severe cases were treated in the community? Moreover, how many less severe cases have been diagnosed and inadequately treated or remain undiagnosed among our nation’s children?
Iron deficiency is not tragic in the sense that cancer, homicide, severe congenital anomalies, and other serious illnesses are during childhood. Iron deficiency is rarely fatal. However, it is surely a tragedy that many millions of children in the world have suffered and are suffering from irreversible brain injury as a result of iron deficiency caused by improper nutritional practices. As Kwiatkowski et al1 indicate, iron deficiency is a multi-system disorder, with profound effects on the central nervous system. Numerous studies during the past 20 years have clearly defined an effect of iron deficiency on mental development and often on motor functioning as well.5, 6 The reduced activity of iron-containing enzymes in the central nervous system leads to deficits that appear, based on animal studies and a number of observations in young children, to be irreversible despite iron therapy.5, 6 It is thus possible that the cumulative effect of preventable IQ loss in children exceeds the more clinically obvious intellectual and motor deficits resulting from disorders such as phenylketonuria, congenital hypothyroidism, galactosemia, and other disorders known to cause brain injury and for which prevention is available. For pediatric hematology-oncology specialists to whom children with severe iron deficiency are often referred, the total deleterious effects on the brain may exceed those encountered in children with leukemia, sickle cell disease, and other disorders in which neurologic complications are well known and often so visible.
It is imperative that pediatricians and other professionals caring for infants and young children be more attentive to good nutritional practices. In particular, everything possible must be done to assure adequacy of iron intake during the first 18 to 24 months of life.7 There are a number of means of assuring iron sufficiency (Table).
Table. Prevention of iron deficiency during infancy and early childhood
| Age <12 mo |
 Avoid whole cow’s milk |
| Encourage breast-feeding |
| Use iron-fortified formula |
| Use iron-fortified infant cereal |
| Age 12 to 36 mo |
| Limit whole cow’s milk intake |
| Limit intake of “regular” cereal (a poor source of iron) |
| Continue iron-fortified cereal |
| Encourage intake of meat and/or iron-rich vegetables (eg, spinach, beans, peas) |
To prevent iron deficiency, exclusive use of an iron-fortified formula for the first 12 months of life is also highly satisfactory. The “low-iron” formulas still used by some practitioners can rarely, if ever, be recommended.8 Other sources of iron include iron-fortified infant cereals (2 half-ounce servings per day easily exceed the daily iron requirement) and ferrous sulfate drops (which are especially useful in premature infants). Whichever of these approaches is used, the most important step is to avoid whole cow’s milk during the first year of life and limit its intake to 16 ounces daily during the second year of life. It is amazing how many parents, and even many primary care physicians, are under the mistaken impression that cow’s milk is the perfect food for growing babies. To paraphrase Dr Frank Oski, one of America’s revered pediatric leaders, “Cow’s milk is for cows, not for children.”9
Not only do we do an inadequate job of preventing iron deficiency, but the diagnostic and treatment approaches used by many physicians are abysmal. Despite managed-care pressures and other constraints, physicians seem to be ordering more tests than ever before. The majority of children referred to me with clear-cut dietary iron deficiency anemia have had a battery of laboratory tests, even though a simple history, hemogram, and response to iron replacement therapy would have clinched the diagnosis and provided treatment as well. Thus, confirmation that the serum ferritin level is low (a result seen only in iron deficiency), that the serum iron level is reduced, and that the serum transferrin level is increased is not generally required to make the diagnosis. As Kwiatkowski et al1 have implied, hemoglobin electrophoresis is also unnecessary in these typical cases, because the results are either normal or do not explain the child’s severe microcytic anemia.
The principles of treatment have been well known for decades. Elemental iron (3 to 6 mg/kg/d) in 2 divided doses (best given as the inexpensive ferrous sulfate drops or elixir) is well tolerated and well absorbed by most infants. I usually recommend the lower dose for mild anemia (hemoglobin >9 g/dL) and the 6 mg/kg/d dose for the more severely affected infants described by Kwiatkowski et al.1 One curious treatment approach that I have seen used by many physicians is the prescription of a vitamin supplement with iron. Many seem to think that the amount of iron in such a daily supplement can correct iron deficiency. This is indeed a misconception. The 10 mg or so of elemental iron contained in each daily vitamin dose is certainly effective in preventing iron deficiency but woefully inadequate as therapy. Yet many children, diagnosed 1 or 2 months previously by their physician as probably having iron deficiency, arrive at our clinic receiving vitamins with iron and with their hemoglobin minimally improved over the baseline.
After initiation of treatment, careful monitoring of patients with iron deficiency is required to assure compliance. In severely affected children, the hemoglobin level should rise by 1 g/dL or more during the first week, and the reticulocyte count should increase as well. By 4 to 6 weeks, even in the most severe cases, the hemoglobin should return to a normal value or nearly so. The erythrocyte red blood cell distribution width index also increases greatly during the first several weeks of therapy (often to 30% or more).
A word about lead poisoning. Many pediatricians consider lead poisoning a common cause of microcytic anemia, as evidenced by the frequent determination of blood lead levels as part of the diagnostic evaluation. Lead certainly inhibits porphyrin synthesis and can contribute slightly to anemia, but it is not a cause of severe microcytic anemia. Actually, it is frequently a result of iron deficiency. Among the behavioral alterations seen in children with iron deficiency is pica. The craving for non-food items has included not only paint chips, dirt, and newspapers but also carpet and the corners of children’s books, and in one case, even the label on the bottle of ferrous sulfate drops that had been prescribed (Figure)!
Figure. Bottle of ferrous sulfate drops, which had been prescribed 1 week earlier to a girl with severe iron deficiency. Two features are apparent. Little of the liquid medication has been used, indicating poor compliance, and the child, whose appetite for paper products was known to be voracious, peeled off and ate the label.
Iron deficiency occurs in infants and young children of all races and ethnic groups. Kwiatkowski et al1 observed that African American children are under-represented in their series, and the relative infrequency of severe iron deficiency in African Americans has been noted by others as well.10 Indeed, the vigorous advocacy and implementation of the WIC Program has clearly had a beneficial impact. There are no Hispanic children in the series by Kwiatkowski et al,1 but in our experience,10 as well as that of others,11 children of Hispanic origin account for 25% or more of patients with severe nutritional iron deficiency anemia. Like the Asian children reported by several groups,1, 10, 12 cultural differences and prolonged bottle feeding, language barriers, and lower socioeconomic status may be causative. Yet severe iron deficiency is not restricted to poor children. Six months ago, I encountered an 18-month-old girl with a hemoglobin level of 2.8 g/dL caused by iron deficiency, resulting from a whole cow’s milk intake of 8 bottles per day, which had begun after 9 months of exclusive breast-feeding. The mother, the recipient of a PhD in psychology, and the father, an engineer, were extremely upset and guilt ridden about their ignorance of optimal nutrition for their child. They stated that their pediatrician had never given them appropriate guidance.
Although iron deficiency during infancy and early childhood is usually due to reduced iron intake, the pediatrician should keep in mind that the primary cause of iron deficiency can occasionally be gastrointestinal hemorrhage,13 malabsorption of iron—which can be due to intrinsic bowel disease, chronic giardiasis,14 or isolated iron malabsorption in an otherwise well child—or intrapulmonary bleeding accompanying idiopathic pulmonary hemosiderosis. These causes can usually be identified by means of history, physical examination, and some simple laboratory tests.
The tragedy of iron deficiency should not occur.7 As recommended by the American Academy of Pediatrics, screening of at-risk term infants should be undertaken between 9 and 12 months of age, and screening of premature infants should begin at 6 months of age. The parents of our patients must be educated, not only by pediatricians but also by advocacy groups, the media, and other health providers such as family physicians, nurse practitioners, physician assistants, and other office staff. If iron deficiency is diagnosed nonetheless, we should minimize laboratory testing, correct underlying causes, and treat without delay. Hopefully, in the future The Journal will no longer receive articles entitled “Severe iron deficiency anemia in young children.”
References
- . Severe iron deficiency anemia in young children. J Pediatr. 1999;135:514–516
- . Continuation of decline in prevalence of anemia in low-income children. The Vermont Experience. Arch Pediatr Adolesc Med. 1997;151:928–930
- . Declining prevalence of anemia in childhood in a middle-class setting: A pediatric success story?. Pediatrics. 1987;80:330–334
- . Iron deficiency in 1- to 3-year-old children. Arch Pediatr Adolesc Med. 1997;151:986–988
- . Iron-deficiency anemia and infant development: effects of extended oral iron therapy. J Pediatr. 1996;129:382–389
- . The liabilities of iron deficiency. Blood. 1986;68:803–809
- . Iron deficiency and anemia. In: Pediatr Basics. 87:Fremont, MI: Publication of Medical Service Department, Gerber Products Company; 1999;p. 2–11
- . Iron-fortified infant formulas. Pediatrics. 1989;84:1114–1115
- . Is bovine milk a health hazard?. Pediatrics. 1985;75(suppl):182–186
- Russell SJ, Wooley R, Buchanan GR. Severe iron deficiency anemia (IDA): a persistent problem for the pediatric hematologist [abstract]. Presented at the Eighth Annual Meeting of the American Society of Pediatric Hematology/Oncology. September 28-30, 1995, Alexandria, VA.
- . Severe iron deficiency anemia (IDA) at the end of the 20th century [abstract]. J Pediatr Hematol Oncol. 1998;20:396
- . Iron status of Asian children aged 2 years living in England. Arch Dis Child. 1998;78:420–426
- . Cows’ milk induced intestinal bleeding in infancy. Arch Dis Child. 1993;68:240–245
- . Iron malabsorption in giardiasis. J Pediatr. 1985;107:75–78
☆ Reprint requests: George R. Buchanan, MD, Department of Pediatrics, University of Texas Southwestern Medical Center at Dallas, 5323 Harry Hines Blvd, Dallas, TX 75235-9063
☆☆ J Pediatr 1999;135:413-5.
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