Iron deficiency anemia in children

Causes of IDA development in children

The etiology of iron deficiency anemia in pediatrics is conveniently systematized chronologically — depending on the period when the negative factor exerted its effect.

1. Antenatal causes (intrauterine). The pathology is associated with impaired formation of iron stores in the fetus. Risk factors include marked iron deficiency in the pregnant woman herself, impaired uteroplacental blood flow, multiple pregnancy with fetal transfusion syndrome, or intrauterine melena. The most important fetal factor is prematurity, since maximum iron storage occurs precisely in the third trimester.
2. Intranatal causes (during childbirth). Caused by impaired blood distribution or acute blood loss during delivery. These include premature clamping of the umbilical cord, depriving the infant of a portion of placental blood, fetoplacental transfusion, as well as bleeding due to birth trauma and umbilical vessel anomalies.
3. Postnatal causes (after birth). Develop due to an imbalance between iron intake and expenditure. Key factors include the alimentary factor (poor dietary intake), growth factor (high rates of somatic development in the first year and during puberty), bleeding, gastroenterological pathologies with malabsorption syndrome, and endocrine shifts of puberty.

Features of metabolism and depletion of stores

The pathogenesis of IDA in early childhood is largely dictated by the mismatch between the huge demands of the growing body and the low exogenous intake of the trace element.

The stores of a term newborn are about 300–400 mg, while a premature infant manages to accumulate only 100–200 mg. In the first days of life, the endogenous pool is supported by physiological hemolysis — the breakdown of fetal hemoglobin (HbF).

Subsequently, iron is supplied via breast milk. Although the bioavailability of the trace element from mother's milk is high, its absolute amount is small. The critical period of store depletion occurs by 5–6 months in term infants and already by 3–4 months in premature infants — at this age, nutrition covers only 25% of the daily requirement. An additional powerful alimentary risk factor is the use of unadapted animal milk (e.g., cow's milk), in which the trace element is critically deficient and poorly absorbed.

The process of iron pool depletion proceeds strictly sequentially. Initially, stores are emptied (ferritin and hemosiderin decrease), and only then does the level of iron in hemoglobin drop.

There are 4 stages of sideropenia development:

• Hypoferremic: iron levels drop, but erythrocytes remain normal.
• Heterogeneous: anisocytosis begins (erythrocytes of varying diameters).
• Microcytic: mean corpuscular volume decreases (microcytosis occurs).
• Anemic: the final stage with clinical manifestation and a drop in hemoglobin levels.

Biochemical classification of iron

In the body, iron exists in two functional forms, the deficiency of which causes a variety of clinical symptoms.

Heme iron (part of the porphyrin ring structure):

• Gas transport: hemoglobin (transport of oxygen and carbon dioxide) and myoglobin (oxygen storage in muscles).
• Respiration and defense enzymes: cytochromes (electron transport) and antioxidant enzymes — catalase and peroxidase.

Non-heme iron:

• Transport and storage: transferrin (plasma carrier), ferritin and hemosiderin (intracellular storage).
• Metabolism: xanthine oxidase (purine metabolism) and dehydrogenases (oxidation-reduction reactions).

Clinical presentation

The symptoms of iron deficiency anemia consist of two syndromes differing in pathogenesis.

1. Sideropenic syndrome Associated with tissue iron deficiency and decreased enzyme activity. Manifests as trophic disorders (dry skin, brittle nails), dyspepsia, and malabsorption syndrome. A specific marker is perversion of smell and taste (Pica chlorotica). The muscular system suffers (hypotonia, myalgia) and secondary immunodeficiency occurs due to the suppression of nonspecific resistance (lysozyme and secretory IgA production drops).

2. Anemic syndrome Caused by hemic hypoxia against the background of decreased hemoglobin. Characteristic features include pallor of the skin and mucous membranes, and rapid fatigue. In infants, psychomotor development delay and tearfulness occur, while in older children, cognitive impairments arise. The cardiovascular system reacts with tachycardia, hypotension, functional murmurs (" venous hum" over the jugular veins, systolic murmur).

Class and exam questions

What else to study on this topic

• Laboratory criteria for latent iron deficiency and IDA
• Specific erythrocyte indices in the diagnosis of anemias
• Mechanisms of iron absorption in malabsorption syndrome
• Differential diagnosis of IDA with other types of anemias in children
• The effect of sideropenia on factors of nonspecific resistance and immunity

Other topics in "Chapter 10. Diseases of the Blood and Blood-Forming Organs"

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