Anemia of prematurity

Classification and stage transition features

Anemic syndrome in infants born prematurely is divided into two interrelated stages — early and late. These forms are not isolated pathologies; they predictably transition from one to the other as the infant's internal compensatory mechanisms are depleted.

During the first months after birth, true iron deficiency often remains hidden. The child's body actively destroys its own red blood cells (hemolysis occurs), and the iron released in the process temporarily masks and compensates for the micronutrient shortage. As soon as these hemolytic reserves are completely depleted, the early form of the disease transforms into the late form.

Early anemia of prematurity

Manifestation of the early form occurs in the 1st–2nd month of life. The disease is primarily characteristic of premature infants, but in clinical practice, it can also occur in full-term newborns if they have a burdened premorbid background.

Clinical symptoms at this stage are quite scarce. The leading and most noticeable diagnostic sign is pronounced pallor of the skin and visible mucous membranes. A laboratory blood test reveals normochromic or hyperchromic anemia of a hyporegenerative nature (i.e., accompanied by a reduced response from the bone marrow).

The etiopathogenesis is based on a specific triad of causes:

1. Enhanced erythrocyte destruction. The life cycle of blood cells is significantly shortened due to morphological anomalies and cell membrane defects. These membrane defects arise primarily against the background of vitamin E deficiency.
2. Suppression of erythropoiesis. The hematopoiesis process suffers due to insufficient production of endogenous erythropoietin. Additionally, iron metabolism is disrupted due to a shortage of important cofactors: specific proteins, vitamin C, and B vitamins.
3. Hemodilution. The intensive growth of a premature infant leads to a rapid increase in circulating blood volume (CBV), which bone marrow hematopoiesis physically cannot keep up with.

Therapeutic tactics for the early form

The foundation of successful patient management is ensuring rational feeding. Medical intervention is based on several key areas:

• Stimulation of erythropoiesis. Used in children with extremely low and very low birth weight (less than 1500 g). Recombinant erythropoietin (epoetin beta) is prescribed at a calculated dose of 200–250 IU/kg. The drug is administered three times a week, and the standard course of therapy is 6 weeks.
• Supplementation. Iron preparations at a dosage of 2 mg/day, as well as vitamin E at a dose of 25 mg/day, are used as supportive treatment.
• Replacement therapy. In severe, life-threatening courses of the disease, red blood cell transfusion is an absolute indication.

Late anemia of prematurity (constitutional)

The late stage of the disease develops in the 3rd–4th month of the child's life. Pathogenetically, it arises as a direct consequence of the complete and final depletion of neonatal iron stores in the body's depots.

In its clinical and laboratory essence, this condition represents a classical variant of iron deficiency anemia (IDA). The disease manifests with typical IDA symptoms, which are usually mild. The examination algorithms, treatment protocols, and prevention methods at this stage are completely identical to those for any other forms of iron deficiency anemia in pediatric practice.

Key aspects of iron metabolism

When evaluating blood parameters, it is important to remember that at the stage of latent iron deficiency, cell morphology does not change immediately. A parameter such as mean corpuscular volume (MCV) does not yet undergo pronounced changes: it may remain within reference ranges or have only a slight downward trend.

When selecting diet therapy (when the child's age allows expanding the diet), it must be taken into account that the most effective source of heme iron with maximum bioavailability is meat.

In some cases, there is a need for parenteral administration of iron preparations (intravenously or intramuscularly, bypassing the gastrointestinal tract). Such tactics are strictly justified if the patient has intestinal pathologies accompanied by malabsorption syndrome and gross impairment of nutrient absorption processes.

Class and exam questions

What else to study on this topic

• Morphological erythrocyte anomalies and membrane defects against the background of vitamin E deficiency.
• The role of cofactors (vitamin C and B vitamins) in the absorption and metabolism of iron.
• Diagnostic criteria for hyporegenerative bone marrow states in newborns.
• Management algorithms for classical iron deficiency anemia (IDA) in infants.
• Indications and rules for red blood cell transfusion in neonatology.

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

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