Iron Deficiency in Infants and Young Children

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Iron deficiency in infants and young childrenAuthorDonald H Mahoney, Jr, MD

Section EditorsKathleen J Motil, MD, PhDJan E Drutz, MD

Deputy EditorMelanie S Kim, MD

Last literature review version 17.3: Setembro 2009 | This topic last

updated: Maro 5, 2009 (More)

INTRODUCTION Iron deficiency (ID) is the most common nutritional

deficiency in children. The World Health Organization estimates that anemia,

largely caused by iron deficiency, affects between 500 million and two billion

people worldwide. In some developing countries, up to 50 percent of preschool

children and pregnant mothers have anemia that principally is caused by iron

deficiency [ 1 ].

In the United States, however, the prevalence of IDA among children has been

declining due to improved iron supplementation [ 2,3 ]. This decline was

illustrated in a report from the Centers for Disease Control and Prevention's

Pediatric Nutrition Surveillance System in Vermont that showed that the

prevalence of anemia between 1981 and 1994 fell from 7.9 to 3.6 percent

(P


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hemochromatosis) and the duodenal iron transporter, rather than urinary or

fecal excretion. In adults, 5 percent of daily iron needs comes from dietary

sources and equals the iron loss that primarily occurs from the gastrointestinal

tract. However, in infants and children, 30 percent of daily iron needs mustcome from diet because of the growth spurt and increase in body (muscle)

mass. (See "Regulation of iron balance" .)

Intestinal iron absorption is a function of three principal factors: body iron stores

(transferrin and ferritin), erythropoietic rate, and bioavailability of dietary iron.

Low iron stores increase receptors in the intestinal mucosa to facilitate increased

iron uptake. Iron absorption also is increased when there is increased

erythropoiesis and reticulocytosis or ineffective erythropoiesis, as in beta

thalassemia. On the other hand, mobilferrin in the intestinal cells can hold onto

iron in the iron replete state; this iron is lost when the mucosal cells are

sloughed. (See "Regulation of iron balance" .)

Heme dietary sources (fish, poultry, and meat) have a higher bioavailability than

do non-heme (vegetable) sources (30 versus 10 percent) ( table 1 ). In addition,

intraluminal factors can affect absorption ( table 2 ). Ascorbic acid enhances the

absorption of non-animal sources of iron such as cereal, breads, fruits, and

vegetables, whereas tannates (teas), bran foods rich in phosphates, and

phytates inhibit iron absorption [ 5-10 ]. Thus, iron deficiency may be a particular

problem in vegetarian children. (See "Vegetarian diets for children", section on'Iron' .)

Developmental aspects Neonates of mothers with iron deficiency are at

increased risk of IDA in early infancy. In one study from India of 55 mothers

with anemia, the iron content of cord blood sample correlated with maternal

hemoglobin and serum ferritin levels [ 11 ]. Breast milk iron was also significantly

reduced in mothers with severe anemia but appeared to be preserved in

mothers with mild-to-moderate anemia.

At birth, term infants have iron stores of approximately 75 mg/kg, two-thirds of

which is bound in hemoglobin. Failure to achieve a normal hemoglobin

concentration (mean 15 to 17 g/dL) at birth directly affects nonstorage iron and

increases the risk for IDA in the first three to six months of life.

During the first five to six months, the normal term infant is iron replete [ 12 ].

However, several conditions in the newborn period can lead to the early

development of IDA:

Prematurity

The administration of erythropoietin (EPO) for anemia of
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prematurity

Fetal-maternal hemorrhage (FMH)

Twin-twin transfusion syndrome (TTS)

Other perinatal hemorrhagic events

Insufficient dietary intake

Premature infants are at increased risk of IDA in early infancy because of a

smaller total blood volume at birth, increased loss through phlebotomy, and poor

gastrointestinal absorption despite decreased ferritin concentrations [ 12 ]. The

use of erythropoietin to prevent and treat the anemia of prematurity further

increases the risk for iron deficiency [ 13 ]. After chronic FMH or TTS, term or

premature infants may develop a microcytic hypochromic anemia early in

infancy as the chronic heme losses prevent the attainment of sufficient iron

stores at birth.

Dietary factors Dietary issues contribute significantly to the evolution of IDA

in infancy and early childhood. Common factors leading to an imbalance in iron

metabolism include [ 14 ]:

Insufficient iron intake

Decreased absorption due to poor dietary sources of iron

Early introduction of whole cow's milk [ 15-19 ]

Occult blood loss secondary to cow's milk intolerance

Medications (eg, aspirin , nonsteroidal antiinflammatory drugs)

Malabsorption states [ 20 ]

Whole cow's milk increases intestinal blood loss in infants. In one study of

infants 5 to 6 months of age, for example, switching to cow's milk increased the

proportion of guaiac-positive stools (from 3 to 30 percent) during the first 28

days, whereas the proportion of positive stools remained low (5 percent) withthe feeding of formula [ 17 ].

In a report from Chile of over 800 infants who were nine months of age, the

prevalence of IDA was highest in infants fed cow's milk formula without added

iron (20 percent), intermediate in the group fed human milk (15 percent), and

much lower in those fed cow's milk formula with added iron (0.6 percent) [ 16 ].

Similar results were seen in an observational study from the Avon Longitudinal

Study of Parents and Children [ 18 ]. In this study, an increased risk of anemia

was associated with either an intake of cows' milk >600 mL/day or >6 breast

feeds/day versus iron-fortified formula in infants at 8 and 12 months. In
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addition, breast milk without iron supplementation has been associated with IDA

in infants at four months of age [ 21 ].

There is an increased risk of iron deficiency with continued bottle-feeding

compared to cup feeding in the second and third year of life (adjusted relativerisk 2.5, 95% CI 2.46-2.53) probably due to greater volumes of cow milk

consumption [ 22 ]. This effect was particularly evident among Mexican American

infants (odds ratio 2.9, 95% CI 1.5-5.6) [ 23 ].

Requirements During childhood, iron stores are primarily determined by

dietary iron intake. This was illustrated in a study of 800 Bolivian mothers and

their children (below five years of age), that demonstrated total body iron stores

were closely correlated between mother and child [ 24 ]. These results underscore

the importance of household dietary iron in determining the iron status of eachfamily member [ 24 ].

Iron requirements in otherwise uncomplicated states approximate 0.5 to 0.8

mg/day. Breast milk contains only 0.3 to 1.0 mg/L iron, but has a high

bioavailability (50 percent); in comparison, proprietary, iron-containing formulas

with 12 mg/L iron have only 4 to 6 percent bioavailability [ 25 ].

Based upon these and other observations, the minimum daily requirements for

iron are [ 5,14 ]:

Full-term infant 1 mg/kg (maximum 15 mg), start no later than

four months in breastfed infants.

Premature 2 mg/kg (maximum 15 mg), start no later than two

months in breastfed infants.

Very low birth weight infants (birth weight less than 1500 g) 3

to 4 mg/kg (maximum 15 mg), start no later than two months in

breastfed infants. In infants with a birth weight of less than 1301 g, one

clinical trial demonstrated that a dose of ferrous sulfate 2 mg/kg per day

started when enteral feedings reach a minimum of 100 mL/kg per day

was safe and potentially beneficial [ 26 ]. Infants who received early

administration of ferrous sulfate had a reduced risk of infection and

number of blood transfusions [ 26 ], and appeared to have a better

neurodevelopment outcome at a median corrected age of 5.3 years [ 27 ].

1 to 10 years old 10 mg/day

11 years old to adult (female) 15 mg/day

11 years old to adult (male) 12 mg/day

Prevention of iron deficiency Recommendations for the prevention of iron
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had iron deficiency and that 3 percent had IDA [ 36 ]. Iron deficiency is higher

among children living at or below the poverty level, among premature or low-

birth-weight infants, among Black and Hispanic toddlers, and among infants fed

only non-iron fortified formulas [ 35,37,38 ].In an analysis of data from the Centers for Disease Control and Prevention's

Pediatric Nutrition Surveillance System (Ped NSS), the prevalence of IDA in low-

income preschool children was 16, 13, 13, and 10 percent for children at 12

months, 18 months, 24 months, and 36 months of age, respectively [ 37 ]. At a

12-month follow-up visit, IDA persisted in 30 percent of patients. The prevalence

of IDA varied with race. Black children had the greatest risk for IDA and were

the most likely to have persistent anemia at 12-month follow-up and Native

American children had the lowest risk for IDA. Asian children had a greater risk

for IDA and persistence of anemia compared to white children but a lower risk

compared to blacks. These results demonstrate the need for ongoing

surveillance and early intervention to prevent iron deficiency during early

childhood in low-income preschool children.

In an analysis of the fourth NHANES survey from 1999 to 2002, risk factors

associated with iron deficiency in children between one and three years of age in

the United States included overweight (defined as weight for height greater than

the 95th percentile for age), Hispanic ethnicity, and not attending day care [ 38 ].

The increasing numbers of immigrants worldwide also creates potential

opportunities for shifts in the prevalence for IDA. This observation was

illustrated in a cohort study of 122 asylum seekers' children in the Netherlands,

where 20 percent of the children had iron deficiency [ 39 ].

SCREENING RECOMMENDATIONS Analysis of the NHANES III database

demonstrated that anemia (hemoglobin level


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sweets, or more than 480 mL (16 oz) of soft drink.

These data provide a framework for who should be screened for iron deficiency

and includes the following screening recommendations by the American

Academy of Pediatrics in infants and young children [ 14 ]:

In normal healthy infants, risk assessment for iron deficiency is

recommended at 4, 18, and 24 months of age, and annually thereafter. A

hemoglobin or hematocrit is recommended at 12 months of age.

Children with special health needs (chronic infection, inflammatory

disorders, chronic gastrointestinal dysfunction, restricted diets).

Children two to five years with increased (dietary) risk factors for

IDA.

The recommendations in adolescents are presented separately. (See "Iron

requirements and iron deficiency in adolescents" .)

In the United States, screening for anemia is generally performed by measuring

hemoglobin/hematocrit between 9 and 12 months. For high risk groups (eg,

those who receive WIC support), blood screening is "mandatory". Follow-up

testing is then mandated at later time periods for those with abnormal results.

Screening for ferritin is more expensive and may miss anemia from

other causes other than IDA.

CLINICAL MANIFESTATIONS Iron deficiency anemia is a microcytic,

hypochromic, hypoproductive state. The features of the natural evolution of this

disorder from storage iron deficiency to iron-limited erythropoiesis to IDA is

shown in Table 4 ( table 4 ). With storage iron deficiency, storage sites are

depleted but sufficient iron remains present within the "labile" iron pool from the

daily turnover of red cells for normal hemoglobin synthesis unless further iron

losses occur. IDA is the last stage in this evolution and, therefore, is the first to

recover with iron repletion.

The most common presentation of IDA is an otherwise asymptomatic, well

nourished infant or child who has a mild to moderate microcytic, hypochromic

anemia ( picture 1 ). Much less frequent are infants with severe anemia, who

present with lethargy, pallor, irritability, cardiomegaly, poor feeding, and

tachypnea.

Although typically presenting as a nutritional anemia, IDA may present as part

of a complex medical problem that includes gastrointestinal blood loss,

malabsorption syndromes, and chronic inflammatory diseases. Examples include
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refractory IDA can be the presenting symptom of celiac disease [ 42 ], IDA may

be associated with helicobacter pylori infections [ 43 ], and IDA is a confounding

finding in anemia of chronic disease [ 44,45 ]. (See "Clinical manifestations and

diagnosis of celiac disease in children", section on 'Iron deficiency' and "Anemiain children due to decreased red blood cell production", section on 'Anemia of

chronic disease' .)

Neurodevelopmental Impaired psychomotor and/or mental development

are well described in iron-deficient infants, and cognitive impairment can occur

in adolescents [ 14,46-48 ]. Iron deficiency may also negatively impact infant

social-emotional behavior [ 49,50 ] and may be a risk factor for children with

attention deficit hyperactivity disorder [ 51 ].

In randomized trials in infants and in toddlers, iron supplementation preventedor corrected impairments in psychomotor development [ 52-56 ]. In one of these

studies, for example, high-risk infants at two months of age were randomly

assigned to receive formula with or without iron. The incidence of iron deficiency

and IDA was significantly higher in nonfortified formula fed infants (53 versus 28

percent) [ 53 ]. Psychomotor development declined in the nonfortified group at 9

and 12 months, but the difference was no longer significant at 15 months.

Mental development and behavior were not affected.

Other studies suggest that psychomotor development may not completely

recover in children with moderate to severe IDA after correction of iron

deficiency [ 54,57,58 ]. In one of these studies, follow-up of individuals enrolled

at 12 to 23 months of age demonstrated the group with chronic iron deficiency

continued to have lower cognitive test scores than those with good iron balance

when evaluated at school-age and adolescence [ 58 ].

Cross-sectional data regarding iron status from the NHANES III (1988-1994)

were compared with standardized test scores for 5398 children aged 6 to 16

years [ 48 ]. Three percent of the children in this sample were iron deficient

(abnormal values for any two of the following: free transferrin saturation,

erythrocyte protoporphyrin, and serum ferritin). Compared to children with

normal iron status, children with iron deficiency had lower average math scores

(93.7 versus 86.4 and 87.4 percent for iron deficient children with and without

anemia, respectively). Reading, verbal, and performance scores did not differ

between the groups.

Iron deficiency in infancy is associated with persistent changes in transmission

through the auditory and visual systems, suggesting that myelination may be

impaired. In one study, auditory brainstem responses (ABR) and visual evoked
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potentials (VEP) were measured at age four years in Chilean children treated for

iron deficiency anemia in infancy and nonanemic controls who also received iron

supplementation [ 59 ]. ABR and VEP latencies were significantly longer in the

children who were formerly anemic compared to controls, suggesting thecontinued presence of subtle auditory and visual dysfunction.

Immunity Iron deficiency in children has been associated with mild to

moderate defects in leukocyte and lymphocyte function, including defective IL-2

and IL-6 production [ 5,60-62 ]. On the other hand, iron is an essential nutrient

for bacterial proliferation. Thus, iron-binding proteins in humans (transferrin and

lactoferrin) have bacteriostatic effects in vitro and demonstrate a competitive

advantage for binding iron over siderophores produced by the organism that

promote iron uptake and organism growth [ 63 ]. However, when the iron-binding

proteins are saturated with iron, the bacteriostatic effect may be lost, with an

increased risk for progression of infection [ 64 ].

Infection In several reports from Africa involving patients with IDA and

protein malnutrition, aggressive treatment with iron resulted in rapid saturation

of iron-binding proteins and reactivation or progression of dormant infections,

such as malaria or tuberculosis [ 64 ]. However, there is no conclusive evidence

that iron supplementation of 1 to 2 mg/day in the immunocompetent host, even

in the face of active infection, is associated with an increased risk for progression

of infection [ 63 ]. In a systematic review of randomized controlled trials, ironsupplementation had no apparent harmful effect on the incidence of infectious

illnesses in children [ 65 ]. However, iron administration increased the risk of

developing diarrhea (IRR 1.11, 95 % CI 1.01-1.23).

Exercise capacity Moderately severe IDA is associated with decreased work

capacity, in part because iron is an essential cofactor for enzyme-driven aerobic

metabolism. Decreased iron, in the absence of anemia, is associated with

decreased exercise performance in laboratory animals. Similar findings have

been noted in children, particularly adolescent athletes. (See "Iron requirementsand iron deficiency in adolescents", section on 'Physical performance' .)

Pica and pagophagia Pica refers to a perverted appetite for substances not

fit as food, such as clay or paper products. Pagophagia, or pica for ice, is

considered quite specific for the iron-deficiency state. It may be present in

children who are not anemic and responds rapidly to treatment with iron, often

before any increase is noted in the hemoglobin concentration [ 66,67 ].

The cause of pica is not known, however, it is most common in children between

the ages of 2 and 3 with developmental disabilities including autism and
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intellectual disability (mental retardation). In addition, pica may also present in

children with brain injury that has affected their development. (See "Diagnosis of

autism spectrum disorders" and "Surveillance and screening for autism spectrum

disorders in primary care" .)Thrombosis Iron deficiency anemia has been reported to be associated with

cerebral vein thrombosis [ 68 ]. In a large case-control study from a

comprehensive Stroke Registry in Canada, previously healthy children with

stroke (arterial or venous) were 10 times more likely to have IDA than healthy

children without stroke [ 69 ]. The mechanisms for this unusual complication are

not clear, but may be related to thrombocytosis (platelet counts approaching 1

million/uL) that can be seen in IDA.

DIAGNOSIS For infants presenting with a mild microcytic anemia and apresumptive diagnosis of IDA, the most cost effective strategy is a therapeutic

trial of iron [ 46 ]. Ferrous sulfate (3 mg/kg of elemental iron, once or twice daily

between meals for four weeks) should produce a rise of greater than 1 gm/dL in

patients with iron deficiency.

Several laboratory tests, most of which can be affected by factors other than

iron status, can be used to confirm the diagnosis of IDA ( table 5 ). Although an

elevated red cell distribution width (RDW) is the earliest hematologic

manifestation of iron deficiency [ 46 ], iron deficiency in infants and young

children usually is identified by a serum ferritin concentration of less than 12

ng/mL and IDA by a hemoglobin concentration below 11.0 g/dL combined with a

low serum ferritin.

In a child thought to be anemic, a complete blood count, with smear and

reticulocyte count, usually is sufficient for screening for the diagnosis of IDA.

Children with a hypochromic microcytic anemia generally are treated with iron,

and further evaluation is performed only if the response is inadequate. A more

complete evaluation for IDA is indicated at presentation in children with

complicated medical histories, which would include serum iron, ferritin, total

iron-binding capacity, and transferrin saturation ( table 5 ). (See

'Treatment' below.)

Other laboratory tests, such as erythrocyte protoporphyrin, serum transferrin

receptor, and reticulocyte hemoglobin content, may prove to be more reliable

measures of iron deficiency, but they are not routinely used [ 70,71 ].

With increasing availability of advanced hematology analyzers, the use of

reticulocyte hemoglobin content may provide a reliable measure of early iron

deficient erythropoiesis. As an example, a prospective observational study of
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202 infants (9 to 12 months of age) demonstrated that reticulocyte hemoglobin

content (CHr) 27.5 pg was a more accurate screen for iron deficiency than a

hemoglobin (Hgb) level 11 g/dL [ 72 ]. There were six patients with iron

deficiency anemia (3 percent) and 23 patients with iron deficiency (11 percent).CHr


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given with juice rather than milk (13.7 versus 5.7 percent absorbed in one

report) [ 75 ].

The estimated cost for this approach in a 10 kg child is approximately five

dollars in the United States. Iron should be continued in responders for two tothree months to replace storage iron pools. If the patient has failed to respond

after four weeks, one should review for medication dosing and administration

errors, appropriate diet modifications, or history of recent illness. Other

laboratory tests, including a serum ferritin, should be obtained to further

evaluate the anemia and to rule out conditions simulating (eg, thalassemias and

the anemia of chronic disease) or complicating (eg, concomitant vitamin B12 or

folic acid deficiency) IDA.

For infants with confirmed IDA, ferrous sulfate (3 to 4 mg/kg of elemental iron,in divided doses, between meals with juice) remains the standard therapy. Iron-

fortified formulas and iron supplementation at these doses are infrequent causes

of gastrointestinal symptoms [ 76,77 ]. Larger doses rarely are necessary and

may produce some degree of intolerance. In patients with severe IDA, a

reticulocyte response may be seen in 72 hours. (See "Oral and enteral iron

supplements: Pediatric drug information" .)

In less-developed countries, simple measures, such as cooking food in iron pots,

may be effective [ 78 ].

Potential causes for recurrent or refractory IDA include:

Compliance failures

Intolerance to medication (fewer than 10 percent as a "true"

cause)

Ongoing gastrointestinal blood loss (parasitic infection, Meckel

diverticulum, ulcers, or other anatomic maladies)

Chronic inflammatory disease

Incorrect diagnosis

Pulmonary hemosiderosis

Parenteral iron therapy There are three different preparations available for

parenteral iron therapy: iron dextran , sodium ferric gluconate , and iron

sucrose (saccharate). Iron dextran is the most commonly used preparation for

pediatric patients. Sodium ferric gluconate and iron sucrose were developed for

use in dialysis patients and are not approved by the US Food and Drug

Administration for use in children.
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The key to reducing the morbidity associated with iron deficiency includes

prevention of iron deficiency and the identification and treatment of children who

are iron deficient.

Prevention Prevention of iron deficiency in infants include ensuring that thedaily intake of iron meets the nutritional requirements of the infant or child. The

dietary recommendations are as follows:

In term infants, breastfeeding exclusively for first four to six

months.

In breastfed preterm or low birth weight infants, elemental iron

supplementation (2 mg/kg per day; maximum 15 mg) is recommended

starting at one month of age and is continued until 12 months of age.

For infants


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1 gm/dL in patients with iron deficiency. (See 'Diagnosis' above.)

Therapy For patients with iron deficiency, oral treatment with ferrous

sulfate (3 mg/kg per day of elemental iron) is recommended. Parenteral therapy

is rarely needed and is reserved for patients with severe, persistent anemia whohave proven intolerance to oral supplements, malabsorption, or poor compliance

to oral therapy. (See 'Our approach' above.)

Use of UpToDate is subject to the Subscription and License Agreement .

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