Anemia in premature babies. A brief plan for dispensary observation of children with IDA. Newborn modb weaver n.n.

It is customary to distinguish between early anemia of prematurity, which appears in the first 2 months. life, and late, arising after 3 months of age, including in the second half of life.

Early anemia of prematurity develops by the end of the 1st month of life, reaches its maximum severity by the 2nd month and then, gradually decreasing, disappears.

The etiology and pathogenesis of early anemia of prematurity is complex and largely unclear. According to G.F. Sultanova (1978), the frequency of toxicosis of pregnant women is not reflected in the frequency of anemia premature babies. However, most authors point to the development of anemia only in children with an unfavorable course of the antenatal period (late prolonged toxicosis pregnant women, exacerbation of chronic foci of infection in the mother during pregnancy, etc.).

In the development of early anemia, the shortened life span of placental erythrocytes, reduced osmotic and mechanical stability of erythrocytes, and the peculiarity of their enzyme spectrum are important.

The cause of early anemia of prematurity in some children may be insufficient folic acid, the reserves of which premature newborn very small. The need for it in a rapidly growing premature baby is great.

^ Clinical picture early anemia of prematurity is characterized by some pallor skin and mucous membranes. With a decrease in hemoglobin concentration below 90 g / l, pallor increases, motor activity and activity during sucking decrease slightly, sometimes a systolic murmur appears at the apex of the heart. However, children continue to still gain weight well. The content of hemoglobin and the number of erythrocytes decreases, there is a tendency to a decrease in the average diameter of erythrocytes and to hypochromia with a decrease in the average hemoglobin content in one erythrocyte. The hematocrit index decreases, the number of reticulocytes in the peripheral blood increases, the concentration of serum iron decreases.

^ Current early anemia in most premature babies is favorable.

Treatment is carried out in accordance with the principles of therapy for IDA in children. Assign iron preparations in a daily dose corresponding to 60-90 mg of elemental iron. Showing vitamins, trace elements.

Late anemia of prematurity develops in children over 3 months of age. It is characterized by all the signs of iron deficiency.

^ Etiology and pathogenesis . The development of late anemia of prematurity is associated with a high need for iron in preterm infants, which is not covered by its intake from outside. Increased absorption of iron in the gastrointestinal tract does not compensate for the need for it, iron deficiency develops in the body, against which anemia occurs.

Clinic. Pallor of the skin and mucous membranes gradually develops, which increases as the anemia progresses. Weakness, lethargy increase, appetite decreases. Anemic hypoxia leads to functional changes internal organs, which is manifested by muffled heart tones, systolic murmur, tachycardia. The content of hemoglobin decreases, hypochromia occurs, as evidenced by the color index (less than 0.8). Gradually decrease the average diameter of erythrocytes and hematocrit value, increases reticulocytosis in the peripheral blood. A blood smear shows microcytosis, anisocytosis, and polychromasia.

Treatment late anemia of prematurity is based on the principle of treatment of iron deficiency anemia in young children. Is of great importance proper organization nursing (walking and sleeping in the fresh air, rational nutrition, massage and gymnastics, prevention of intercurrent diseases, etc.). Iron preparations, vitamins, trace elements are prescribed. Intravenous administration of iron to premature infants is not indicated due to possible poisoning, the likelihood of which is not excluded due to the low concentration of transferrin in them.

Blood transfusions for the treatment of late anemia of prematurity are used only in exceptional cases (severe anemia, acute large blood loss, severe condition due to infection).

Brief plan for dispensary observation of children with IDA

1. 
   The duration of dispensary observation is 1 year.
2. 
   Review by pediatrician monthly for the first 3 months after normalization of Hb, then quarterly.
3. 
   Consultation of a hematologist and other medical specialists according to indications.
4. 
   Laboratory research:

• 
  complete blood count 1 time per month - the first 3 months, then 1 time in 3 months;
• 
  urinalysis 1-2 times a year;
• 
  blood test for serum iron - according to indications.

1. 
   Therapeutic and preventive and health measures:

• 
  Rational mode with age characteristics physical education and sufficient exposure to fresh air.
• 
  Balanced diet.
• 
  Ferrotherapy.
• 
  Premature babies, children from multiple pregnancies from 3 months of life to the end of the first half of the year are recommended to take iron preparations at a dose equal to 1/3 - 1/2 of the daily therapeutic dose.
• 
  Vitamins B 1, B 2, B 6, C in age-specific physiological doses for 2-3 weeks 2 times a year.

1. 
   Preventive vaccinations are allowed at Hb levels of at least 100 g/l for deficiency anemia mild degree, in other cases, vaccinations are carried out after the normalization of Hb.

^ CHRONIC NUTRITIONAL DISORDERS

IN YOUNG CHILDREN

Chronic eating disorders in young children, according to the classification of G.A. Zaitseva and L.A. Stroganova (1981, 1984) are represented by malnutrition (lagging body weight behind height), hypostatura (uniform lag in weight and height) and paratrophy (excess weight).

The most relevant and difficult to manage on pediatric area children are underweight. In this regard, we will focus on the problem of observation and treatment of children with malnutrition and hypostatura.

Hypotrophy(HT) (E40-E46) is a multifactorial disease characterized by body weight in relation to length and associated with insufficient intake of nutrients, impaired absorption and utilization.

According to the time of occurrence, prenatal (intrauterine) and postnatal (intrauterine) forms of malnutrition are distinguished.

Establishing the leading etiological factor in the development of HT is extremely important for the organization of preventive and therapeutic measures. So, the most common causes of intrauterine HT are unbalanced or malnutrition pregnant women, constitutional features of the mother, young or “old” age of the woman in labor, all somatic diseases and complicated pregnancy leading to the development of chronic fetoplacental insufficiency and intrauterine hypoxia, occupational and domestic hazards, stressful situations, taking medications, pathology of the placenta and umbilical cord, intrauterine infections.

Postnatal HT develops under the influence of both exogenous and endogenous causes, which determines the corresponding division of postnatal HT forms. Exogenous causes include qualitative and quantitative feeding defects suffered infectious diseases, especially the intestines, toxic effects, violations of child care. Endogenous causes include congenital malformations of organs and systems (for example, congenital heart disease, anomalies digestive system, nervous system), hereditary metabolic anomalies, malabsorption syndrome, immunodeficiency states, endocrinopathies, chromosomal diseases.

Main diagnostic criteria hypotrophy:

• 
  consistent disappearance or reduction of the subcutaneous fat layer on the abdomen, chest, limbs, face;
• 
  underweight, and in severe cases, stunting;
• 
  decrease in tissue turgor;
• 
  a decrease in food tolerance, manifested by a decrease in appetite, regurgitation, vomiting, dyspeptic stools;
• 
  decrease in resistance to the effects of infectious and other agents;
• 
  signs of polyhypovitaminosis;
• 
  catabolic orientation of metabolic processes.

It must be emphasized that the diagnosis of HT is clinical and is based not only on mathematical calculations of the percentage of mass deficiency, but on a whole complex of symptoms.

Laboratory examination of a patient with HT at the pediatric site includes a complete blood count, urine, coprogram, stool culture, examination of the intestinal biocenosis; in a hospital, these methods are supplemented by the determination of blood glucose, a proteinogram, an ionogram, urea, CBS, an immunogram and a number of instrumental methods to exclude endogenous factors of malnutrition (for example, ECG, EchoCS - for the diagnosis of CHD, radiography of the heart, fibrogastroscopy, radiography of the digestive system - for diagnosis of anomalies of the digestive system, etc.)

Treatment of hypotrophy I stage. carried out in outpatient settings. Severe HT (I, II stage), the presence of other somatic diseases, unfavorable social and living conditions serve as indications for hospitalization of the patient.

Treatment of a patient with HT should be comprehensive and include the elimination of the causes of malnutrition or their correction, diet therapy, the organization of a rational daily regimen and care, the identification and treatment of chronic foci of infection and concomitant diseases. Drug therapy is built taking into account the main links of pathogenesis, namely:

• 
  the reduced enzymatic activity of all glands of the gastrointestinal tract is taken into account;
• 
  as the disease progresses, dysfunctions of the subcortical formations of the central nervous system occur;
• 
  polyhypovitaminosis develops;
• 
  metabolic processes have a catabolic orientation, which leads to the development of metabolic acidosis;
• 
  water and electrolyte metabolism is disturbed with the development of dehydration, hyponatremia, hypokalemia, hypocalcemia;
• 
  there are dystrophic changes in the cardiovascular, respiratory, urinary systems, liver, endocrine glands.

Treatment of a child with HT should be carried out against the background of the most sparing regimen. The child should be protected from unnecessary irritants, provide maternal care, optimal microclimate (t = 25-27С, humidity 60-70%, frequent ventilation), during walks the child should be in his arms. The use of massage and gymnastics is carried out at the stage of reparation, when the child is steadily gaining weight. Showing water procedures(salt-coniferous baths).

The basis of successful treatment of HT is diet therapy.

With GT I Art. food tolerance is quite high, children tolerate food loads well. To ensure high needs for food ingredients, proteins are prescribed at the rate of 4-4.5 g / kg, fats - 6-6.5 g / kg / day, carbohydrates - 14-16 g / kg / day, calories - 140-160 kcal /kg/day The calculation of all nutrients is carried out on the actual body weight, which greatly facilitates mathematical calculations.

The amount of food is also calculated on the actual weight, the number of feedings does not change, the subsidy of nutrients is provided by the appointment of cottage cheese, kefir, protein and fat enpits, sugar syrup.

Drug therapy for GT I st. limited to the appointment of enzymes and vitamins inside to improve the digestion and assimilation of food.

In the treatment of GT II-III Art. distinguish 2 periods:

I - the stage of determining food tolerance (the phase of minimal nutrition, pre-reparation);

II - stage of enhanced nutrition (phase of optimal nutrition, reparative).

Requirements for proteins, fats, carbohydrates, calories in HT (N.I. Aleksandrova et al., 1990) are presented in the table.

The calculation is based on the actual body weight.

The main goal of the minimum nutrition stage is to remove from the body substances accumulated as a result of the predominance of catabolic processes of adaptation of the patient to gradually increasing nutritional loads, restore the activity of digestive enzymes and, as a result of the foregoing, restore food tolerance.

The duration of the stage of minimal nutrition with GT II st. - 5-7 days, with GT III Art. - up to 14 days. The principle of diet rejuvenation is used, i.e. the frequency of feeding increases (with GT II stage - after 3 hours, with GT III stage - after 2-2.5 hours), the daily volume of enteral nutrition decreases (with GT II stage - up to 2/3 of age norm, with GT III Art. - up to 1/3 of the age norm).

Preferably at stage I is the use of breast milk or adapted milk formulas, preferably fermented milk.

The missing fluid volume is replenished by parenteral nutrition using solutions of amino acids (Levamin, Alvezin, Vamin), fat emulsions (Intralipid, Lipofundin) and 10% glucose solutions. Partial parenteral nutrition is carried out in a hospital, requires careful biochemical control and prevention of complications (metabolic, septic, technical). Indications for the appointment of partial parenteral nutrition are malnutrition II-III stage, mainly of endogenous origin, with a progressive course of the disease in children with a sharply reduced food tolerance.

In other cases, the fluid deficiency is replenished by enteral administration of solutions such as rehydron, glucosolan.

The amount of enterally administered nutrients increases daily. After the child begins to cope with the proper amount of nutrition, the activity of gastrointestinal enzymes is restored, the emotional tone improves, the dyspeptic syndrome is stopped, the coprogram is normalized, and they move on to stage II - enhanced nutrition.

Gradually, low-calorie mixtures are replaced with mixtures containing a sufficient amount of protein and fat (“Detolact”, “Enfamil”, “Semilak”, etc.).

The required amount of carbohydrates is provided by the introduction of juices, fruit puree, complementary foods. Biologically valuable additives to puree, porridge are egg yolk, vegetable and butter, cream, and later, taking into account the age of the child - liver, minced meat. You can introduce complementary foods only with a positive dynamics of body weight. The timing of the introduction can be shifted 2-3 weeks earlier than traditional, each the new kind food is administered under the control of the coprogram. Control over diet therapy and its correction is carried out by calculating nutrition 1 time in 7-10 days and a coprogram.

At the stage of enhanced nutrition, an increase in the protein quota is achieved by the appointment of cottage cheese, kefir, protein enpit. To increase the fat load, fat enpit, 10% cream, butter, correction of carbohydrate content is used - due to sugar syrup.

Drug therapy for HT depends on the stage of treatment.

At the 1st (stage of minimal nutrition) enzyme therapy is used. It is preferable to use the following drugs: pancreatin 0.1 x 3 r., Abomin 0.05 x 3 r., orase 1/2-1 tsp, creon granules 1 caps. / day - for 1 month. The use of drugs such as festal, digestal, panzinorm is limited due to unacceptable crushing of the tablet due to the uneven distribution of granules in it, as well as due to the content of bile acids and hemicellulose in these drugs.

Vitamin therapy in the treatment of malnutrition is used for replacement and stimulating purposes. In the first days of treatment, vitamins are administered parenterally, then orally. The following drugs are used in a course of 2 weeks to 1 month:

• 
  ascorbic acid 0.05 - 0.1 / day;
• 
  vit. In 1 0.0025 - 0.005 / day;
• 
  vit. At 6 0.001 - 0.003 / day;
• 
  vit. A 3.44% oil solution - 1 cap. in one day;
• 
  vit. B 5 0.005-0.01/day;
• 
  vit. At 15 0.05 / day, divided into 3 doses;
• 
  nicotinamide 0.005 - 0.01 x 2-3 r.

At the II stage of treatment with an anabolic purpose, the appointment of Vit. B 12 or its coenzyme form (cobamamide (0.25 mg / kg. day), potassium orotate - 10-20 mg / kg / day in monthly courses. Upon reaching enough fats in the daily diet in order to improve its absorption, a 20% solution of carnitine chloride is prescribed, 20-30 drops each. per day for 14 days. In order to reduce lipid peroxidation, antioxidant therapy is carried out (vit. E, A, C).

At the second stage, stimulating therapy is also indicated: apilac 2.5-5 mg in suppositories x 1 time per day No. 14; dibazole 0.5 mg/year of life x 3 times a day; plant adaptagens are used - tinctures and decoctions of eleutherococcus, ginseng, aralia, zamanihi, leuzea (in a single dose of 1 cap. / year of life 2 times a day).

To normalize the intestinal microbiocenosis, depending on the identified violations, specific phages are used (coli-proteus, anti-staphylococcal, pyophage, bacteriophage-intesti). Biological preparations (bifidum-bacterin, lactobacterin, acipol, bifacid, hilak) are effective.

In order to improve the functional state of the liver, hepatoprotectors are used - Essentiale, legalon, carsil, lipoic acid, methionine, lipamide.

The appointment of anabolic steroids should be carried out according to individual indications in the form of HT that is resistant to therapy, under the control of the hormonal blood profile. Nerabol 0.1 - 0.3 mg / kg.day, retabolil 1 mg / kg x 1 r in 2-3 weeks, thyroidin 0.01 - 0.03 x 2 r are used. per day.

The prognosis for the success of HT treatment is largely determined by its cause and the possibilities for its elimination (for example, radical correction birth defect hearts). Approximate terms of withdrawal from the HT state can be calculated based on the fact that with properly organized treatment, the child monthly gives an increase in weight, 200-300 g more than the age.

Prevention of malnutrition carried out, starting from the antenatal period, together with obstetrician-gynecologists. The main directions of this work:

• 
  rational nutrition of a pregnant woman (fasting days are absolutely contraindicated);
• 
  treatment of somatic and urogenital diseases;
• 
  exclusion of occupational hazards, stressful situations, bad habits;
• 
  treatment and prevention of complicated pregnancy and childbirth.

Postnatal prophylaxis includes:

• 
  natural feeding with its timely correction;
• 
  rational mixed and artificial feeding;
• 
  optimal nutrition for a nursing mother;
• 
  complete childcare;
• 
  prevention and treatment of gastrointestinal diseases.

Treatment and monitoring of patients with HT - an examination for the professional suitability of a pediatrician. The main principles were and remain patience, perseverance, moving forward with slow steps.

^ A brief plan for dispensary observation of children,

undergoing malnutrition

1. 
   The duration of dispensary observation is 1 year
2. 
   Frequency of examination by a pediatrician with obligatory weighing at least 1 time in 2 weeks.
3. 
   Consultations of a neuropathologist, an oculist, and in some cases an endocrinologist - according to indications.
4. 
   Laboratory examination:

• 
  general analyzes blood, urine - 1 time in 3 months in the first year of life and with a continuing risk of malnutrition in the 2nd year of life;
• 
  coprogram - according to indications.

1. 
   Monitoring the neuropsychic development of the child.
2. 
   Preventive and therapeutic measures:

• 
  Optimal Nutrition nursing mother.
• 
  Maximum preservation of natural feeding. If necessary, control feeding at least 3 times during the day at home in the presence of scales.
• 
  Rational mixed and artificial feeding using adapted mixtures, calculation of nutrition and its correction 1 time per month during the dispensary observation.
• 
  Timely introduction of complementary foods.
• 
  Carrying out year-round specific and non-specific prevention of rickets.
• 
  Drug therapy according to indications, depending on the clinical form of malnutrition (biological products, vitamins, enzymes, hepatoprotectors, stimulating therapy).

1. 
   Preventive vaccinations are allowed with persistent weight gain.

^ ANOMALIES OF THE CONSTITUTION

A special place in the pathology of children, especially at an early age, is occupied by anomalies of the constitution.

Anomaly of the constitution - this is a state of the body, which is characterized by a special adaptability of the body to environmental conditions, a kind of reactivity, a predisposition to a number of diseases and to a peculiar course of pathological processes.

Currently, we identify the concept of an anomaly of the constitution and diathesis. Although Speransky pointed out that diathesis, as a concept, is much narrower, and understood by it only a predisposition to certain diseases.

The doctrine of constitutions and their anomalies has evolved. And although different authors distinguish about 17 types of diathesis, the more studied are: exudative-catarrhal diathesis, lymphatic-hypoplastic, neuro-arthritic, allergic, hemorrhagic.

It must be emphasized that since anomalies of the constitution are not diseases in the literal sense, then there are no such concepts in the international classification of diseases. However, under certain conditions, diathesis is transformed into very specific nosological forms.

^ EXUDATIVE-CATARIAL DIATHESIS

ECD is a combination of congenital and acquired features of the body, characterized by an abnormal reaction to the action of both conventional and pathogenic stimuli: a tendency to develop inflammatory processes in the skin and mucous membranes, a decrease in overall immunoreactivity, a violation of neuroendocrine adaptation and metabolism. Frequent allergic reactions, polymorphic rashes. The frequency of occurrence is 30 - 75%.

Etiology. Allergy plays a leading role in the etiology and pathogenesis of ECD. The sensitization of the child goes mainly by food.

Most often, proteins and their compounds with carbohydrates (glycoproteins) and fats (lipoproteins) act as allergens. These are substances added to food to improve its organoleptic properties: dyes, aromatic additives (salicylates, menthol), emulsifiers, preservatives (sulfur dioxide, sodium benzoate), enzymes synthesized by fungi, mold. As well as fertilizers and pesticides in vegetables, fruits, cereals, migration products from polymer and metal packaging (nickel)

Obligate allergens include milk, meat, fish, chocolate, nuts, citrus fruits, strawberries, honey.

Optional allergens are substances containing endogenous histamine: sauerkraut, spinach, cheeses, sorrel, pork liver, sausages, sausage, ham, tomatoes, soybeans, strawberries, hazelnuts, and histamine liberators that release histamine by activating the complement system: alcohol , smoked meats, fish, pickled herring, raspberries, eggs, mushrooms, spices, tomatoes, citrus fruits, banana, brewer's yeast, coffee, strawberries, strawberries.

Premature is considered to be children born in the period from the 22nd to the 37th week of gestation with a body weight of less than 2500-2700 g and a body length of less than 45-47 cm. The most stable indicator is the gestational age.

The fetus is viable (according to WHO definition) with a body weight of 500 g or more, a body length of 25 cm or more, and with a gestational age of more than 22 weeks. National statistics of Russia on miscarriage (spontaneous termination of pregnancy at a period of less than 37 full weeks) takes full account of these recommendations. Statistics on prematurity (spontaneous or induced termination of pregnancy from the time when the fetus is considered viable) among live births takes into account only children from the 28th week of gestation weighing 1000 g or more and body length 35 cm or more. Of those born alive with a body weight of 500-999 g, newborns who lived 7 days after birth are subject to registration.

The number of premature babies in different countries ranges from 3 to 17%, in Russia - 3-7%. Among prematurely born children, the highest morbidity and mortality are observed. They account for about 75% of infant mortality in our country; in the most economically developed countries - 100%.

CAUSES OF PREMATED BIRTH OF CHILDRENMain reasons premature birth children are next.

Socio-biological factors.

Parents too young or too old. If old age has a negative effect on gestation due to biological changes in the aging body, then the birth of premature babies in young mothers is due to unplanned pregnancies.

Miscarriage is influenced by the low level of education of parents and the associated unhealthy lifestyle during pregnancy and a lack of understanding of the importance of constant

medical supervision. Among children born to women who were not observed during the entire pregnancy in antenatal clinic, the perinatal mortality rate is 5 times higher.

play an important role in miscarriage occupational hazards, bad habits, hard physical labor. Not only the mother, but also the father has a negative impact on the health of the child. Severe malformations in children from men who smoke for many years and / or smokers a large number of cigarettes occur 2 times more often than in children from non-smoking fathers.

Even with a desired pregnancy, the risk of miscarriage in single women is higher than in married women, which is due to social and psycho-emotional factors.

previous abortions. The complete elimination of abortion with the use of effective contraception can reduce the rate of preterm birth by 1/3.

Short intervals between births (less than 2 years) may be the cause of premature delivery.

Mother's illnesses.

pathological course of pregnancy.

DEGREES OF PREMATURITY

There are four degrees of prematurity (Table 4-1).

Table 4-1.Degrees of prematurity

Currently, the diagnosis usually does not indicate the degree of prematurity, but the gestational age in weeks (a more accurate indicator).

SIGNS OF PREMATURITY Clinical signs

The appearance of a premature baby depends on the degree of prematurity.

Deep premature baby(body weight less than 1500 g) has a thin wrinkled skin dark red in color, richly covered with cheese-like grease and fluff (lanugo). simple erythema

lasts up to 2-3 weeks. The subcutaneous fat layer is not expressed, the nipples and areolas of the mammary glands are barely visible; auricles are flat, shapeless, soft, pressed against the head; nails are thin and do not always reach the edge nail bed; the navel is located in the lower third of the abdomen. The head is relatively large and is 1/3 of the body length; limbs are short. The sutures of the skull and fontanelles (large and small) are open. The bones of the skull are thin. In girls, the genital slit gapes as a result of underdevelopment of the labia majora, the clitoris protrudes; in boys, the testicles are not descended into the scrotum.

In more mature premature babies, the appearance is different. Leather Pink colour, there is no fluff on the face (at birth on the 33rd week of gestation), and later on the trunk. The navel is located slightly higher above the womb, the head is approximately 1/4 of the body length. In children born after 34 weeks of gestation, the first bends on the auricles appear, the nipples are more visible and areola, in boys, the testicles are located at the entrance to the scrotum, in girls, the genital slit is almost closed.

Premature infants are characterized by muscle hypotension, decreased physiological reflexes, decreased motor activity, impaired thermoregulation, and weak crying. A deeply premature baby (less than 30 weeks of gestation) lies with outstretched arms and legs; sucking, swallowing and other reflexes are absent or weakly expressed. Body temperature is unstable (it can drop to 32-34? C and rises easily). At birth after the 30th week of gestation, a premature baby is found to have partial flexion of the legs at the knee and hip joints; sucking reflex is good. In a child born at 36-37 weeks of gestation, flexion of the limbs is complete, but unstable; a distinct grasping reflex is elicited. A premature baby in the first 2-3 weeks of life may have a non-permanent tremor, non-rough and non-permanent strabismus, horizontal nystagmus with a change in body position.

Premature boys and girls do not differ in anthropometric parameters, since these differences are formed in the last month of pregnancy (full-term boys are larger than girls).

Features of internal organs

Morphological and functional immaturity of the internal organs is also in line with the degree of prematurity and is especially pronounced in very preterm infants.

Breathing in premature babies is superficial with significant fluctuations in respiratory rate (from 36 to 76 per minute), with a tendency to tachypnea and apnea lasting 5-10 seconds. In children born at less than 35 weeks of gestation, the formation of surfactant is impaired, which

ry prevents the collapse of the alveoli on exhalation. They develop SDR more easily.

Heart rate in premature babies is characterized by high lability (from 100 to 180 per minute), vascular tone is reduced, systolic blood pressure does not exceed 60-70 mm Hg. Increased permeability of the vascular walls can lead to impaired cerebral circulation and cerebral hemorrhage.

Due to the insufficient maturity of the renal tissue, its function to maintain acid-base balance is reduced.

All gastrointestinal enzymes necessary for the digestion of breast milk are synthesized, but are characterized by low activity.

In preterm infants, there is no relationship between the intensity of jaundice and the degree of transient hyperbilirubinemia, which often leads to an underestimation of the latter. The immaturity of the liver and the associated insufficient activity of the enzyme glucuronyl transferase, increased permeability of the blood-brain barrier (BBB), as well as the rapid breakdown of erythrocytes can lead to the accumulation of indirect bilirubin in the blood in the first days of life and the development of bilirubin encephalopathy, even at a relatively low concentration of bilirubin (170-220 µmol/l).

Laboratory research

In the first days of life, premature babies are more likely than full-term babies to have hypoglycemia, hypoproteinemia, hypocalcemia, hypomagnesemia, hyperkalemia, and decompensated metabolic acidosis. The content of erythrocytes and Hb at birth is almost the same as in full-term, but the content of HbF is higher (up to 97.5%), which is associated with intense hemolysis. From the second day of life, red blood values ​​change at a faster pace than in full-term ones, and at the age of 6-8 weeks, a typical deviation in the hemogram appears for premature babies - early anemia of prematurity. The leading cause of anemia is considered to be low production of erythropoietin. The content of leukocytes is the same as in full-term children, however, the presence of young forms up to promyelocytes is typical. The first crossing of granulocytes and lymphocytes occurs the later, the greater the degree of prematurity (with III degree - by the end of the first month of life).

PECULIARITIES OF THE DEVELOPMENT OF PREMATURE CHILDREN Physical development

The physical development of preterm infants is characterized by a higher rate of increase in body weight and length during the first year.

life. The smaller the weight and length of the body of a premature baby at birth, the more intensively these indicators increase during the year.

By the end of the first year of life, body weight increases as follows: with prematurity IV degree 8-10 times, III degree - 6-7 times, II degree - 5-7 times, I degree - 4-5 times. Body weight increases unevenly. The first month of life is the most difficult period of adaptation, especially for a very premature baby. The initial body weight decreases by 8-12% (in full-term children by 3-6%); recovery is slow. With a gestation period of less than 32 weeks, body weight often reaches its initial values ​​only by the end of the first month of life and begins to increase more intensively from the 2nd month.

The body length of a premature baby by the end of the first year of life is 65-75 cm, i.e. increases by 30-35 cm, while in a full-term one, the body length increases by 25 cm.

Despite the high rates of development, in the first 2-3 years of life, premature babies lag behind their peers who were born full-term. Alignment occurs after the third year of life, often at 5-6 years. In the future, in children born prematurely, asthenia and infantilism are often observed, but indicators of physical development characteristic of full-term peers are also possible.

psychomotor development

In psychomotor development, healthy premature babies compare with their full-term peers much earlier than in physical development. Children with II-III degree prematurity begin to fix their eyes, hold their heads, roll over, stand up and walk on their own, pronounce the first words 1-3 months later than full-term ones. Premature babies "catch up" with full-term peers in terms of psychomotor development in the second year of life; with prematurity I degree - by the end of the first year.

FEATURES OF NURSING PREMATURENursing of premature babies is carried out in two stages: in the maternity hospital and in a specialized department. Then the child comes under the supervision of the clinic.

All over the world, great importance is attached to the "soft nursing of premature babies" with the limitation of intensive care, stressful situations, pain. After the birth of a premature baby, it should be placed in a sterile warm diaper (“optimum comfort”). Cooling immediately after birth, while still in the delivery room, often dooms all further care to failure. So, if the body temperature of a premature baby only once dropped to 32? C

and below, mortality reaches almost 100%, even with the correct use of all modern methods of care and treatment in the future. In the first days of life, very premature babies or premature babies in a serious condition are kept in incubators. They maintain a constant temperature (from 30 to 35 ° C, taking into account the individual characteristics of the child), humidity (on the first day up to 90%, and then up to 60-55%), oxygen concentration (about 30%). The child's body temperature can also be maintained in a heated crib or in an ordinary crib using heating pads, since the longer the stay in the incubator, the more likely child infection. The optimum air temperature in the room is 25?C. It is necessary to support the adaptive reactions of the child by instilling native mother's milk into the mouth from a pipette, heated diapers, prolonged stay on the mother's chest (like "kangaroo"), a calm voice nurse, stroking movements of her hands.

From maternity hospital Only 8-10% of healthy premature babies with a birth weight of more than 2000 g are discharged home. The rest are transferred to specialized institutions for the second stage of nursing.

FEATURES OF PREMATURE FEEDING

Feeding characteristics of preterm infants are due to their increased need for nutrients due to intensive physical development, as well as functional and morphological immaturity of the gastrointestinal tract, and therefore food should be introduced carefully. Even deeply preterm infants should be fed already in the first hours of life due to the catabolic orientation of metabolism, hypoproteinemia and hypoglycemia.

With parenteral nutrition, the child's intestines are quickly colonized by conditionally pathogenic microflora. At the same time, the permeability of the mucous membranes of the gastrointestinal tract increases, which contributes to the generalization of the infectious process. Parenteral nutrition is resorted to only in extremely severe conditions in very premature babies and for a limited period of time. It is more expedient for such children to prescribe round-the-clock drip administration of native mother's milk.

Children with gestational age more than 28 weeks, as well as all preterm infants with SDR, a weak sucking reflex, breast milk is administered through a gastric tube. With satisfactory general condition, quite pronounced sucking reflex and body weight at birth more than 1800 g can be applied to the breast in 3-4 days. Preterm infants with a birth weight of less than 1500 g are breastfed from the third week of life. In the absence of milk from the mother, specialized mixtures are prescribed for premature babies.

(for example, "Nenatal", "preNAN", etc.) Upon reaching a body weight of 2500-3000 g, the child is gradually transferred to conventional substitutes for women's milk.

Nutrition calculations are made in accordance with the need of the child's body per 1 kg of body weight per day: 1-2nd day of life - 30 kcal, 3rd day - 35 kcal, 4th day - 40 kcal, then 10 kcal more daily up to the 10th day of life; on the 14th day - 120 kcal, from the 21st day of life - 140 kcal.

When determining the volume of food, one should take into account the individual characteristics of the child: very premature babies from the 2nd month sometimes absorb the volume of breast milk corresponding to 150-180 kcal/kg.

LONG-TERM CONSEQUENCES OF PREMATUREAmong premature babies, the risk of mental and physical disability is higher than among full-term babies.

Severe neuropsychiatric disorders in the form of cerebral palsy, intellectual decline, hearing and vision impairment, epileptic seizures occur in 13-27% of premature babies.

Premature babies are 10-12 times more likely to have malformations. They are characterized by a disproportionate development of the skeleton, mainly with deviations towards asthenia. Many of them have an increased risk of "school maladjustment" in the future. Among those born prematurely, attention deficit hyperactivity disorder is more often observed.

In women who were born very premature, in the future, violations are often observed menstrual cycle, signs of sexual infantilism, the threat of abortion and premature birth.

Despite the above, with proper care and rational nutrition, premature babies usually grow up healthy and become full members of society.

PREVENTIVE BIRTH OF CHILDRENPrevention of premature birth of children provides for the protection of the health of the expectant mother; prevention of medical abortions, especially in women with menstrual irregularities and neuroendocrine diseases; creation of favorable conditions for pregnant women in the family and at work; timely identification of risk groups and active monitoring of the course of pregnancy in these women.

In premature babies, the body has not yet fully matured. Therefore, he is not adapted to independent existence. The qualitative and quantitative composition of the blood in such children will differ in a number of features. Even under the condition normal development, the absence of disease in premature babies develops anemia.

Features of the blood of premature babies:

In premature babies, the hemoglobin level and the number of red blood cells may be the same as in full-term babies. Rarely, there is a decrease or, conversely, an increase in these indicators. During the first two months of life, there is a rapid decrease in the amount of hemoglobin in the blood. The speed of this process is much higher in premature babies than in full-term babies. As a result, a condition develops that is characteristic of children born prematurely. In medicine, it is called anemia of premature babies.

Causes of anemia in premature babies:

Currently, there are several theories of anemia in premature babies. The main ones suggest the following reasons:

Lack of iron in the child's body, which is necessary for the synthesis of hemoglobin. It has been established that this is not the only reason diseases. Often, with the introduction of iron preparations in the first weeks of a child's life, they do not give positive results.
metabolic disorders in the body
decreased iron stores in the body
maternal anemia
the rapid increase in body weight of the child in the first months of life. This factor leads to increased iron requirements.
lack of enzymes that are involved in the synthesis of hemoglobin
elevated level bilirubin in the blood, which leads to increased breakdown of red blood cells
temporary functional insufficiency of the bone marrow - the main organ where red blood cells are produced
congenital diseases, especially sepsis
pathologies acquired for the first time in the life of a premature baby: rickets, pneumonia, infectious diseases
improper and irrational nutrition of the child, late introduction of complementary foods and supplementary feeding. Foods containing insufficient amounts of proteins and vitamins often increase the manifestations of anemia in premature babies.
unfavorable hygiene conditions
lack of fresh air
unfavorable ecological situation

Timing of anemia in premature babies:

At normal course pregnancy, proper development of all internal organs and systems, any premature baby will show signs of anemia of varying degrees.

The active manifestation of the symptom of the disease begins at the end of the first - the beginning of the second month of the child's life. The peak of anemia is noted, as a rule, at 3-4 months of age. If you provide proper care for the baby, as well as adhere to dietary norms, use effective drugs, the manifestations of the disease completely disappear at the age of 6-7 months.

Important! If anemia in a premature baby persists for more than 7 months, then other causes of the disease that are not related to the premature birth of the baby should be looked for.

Symptoms of anemia in premature babies:

The main symptom of anemia is a decrease in the level of hemoglobin in the blood and the number of red blood cells. This leads to a deterioration in the supply of oxygen to the child's body. Developing manifestations of hypoxia - oxygen starvation. All organs and systems suffer from this: the cardiovascular, respiratory, nervous systems, which are extremely sensitive to a lack of oxygen in the child's blood. The manifestations of such violations can be the following:

Cardiopalmus. This is a compensatory reaction, due to which more blood flows to organs and tissues and oxygen supply improves.
an increase in the size of the heart due to constant overload
characteristic changes on the cardiogram
myocardial hypoxia
shortness of breath, shortness of breath. With a mild degree of anemia, this sign appears only during exercise. With more severe forms anemia dyspnea develops at rest
shallow, shallow breathing
hyperexcitability of the child
child's depression
apathy
lack of reactions to external stimuli in severe forms of anemia
deterioration or complete loss of appetite
pallor of the skin
pallor of mucous membranes
an increase in the size of the spleen with hemolytic anemia associated with increased breakdown of red blood cells
decrease in the level of iron in the blood test with iron deficiency anemia
frequent regurgitation
dry skin
stool disorders
swelling of the face and limbs in severe forms of anemia
lagging behind in physical and mental development
increased susceptibility to infectious and inflammatory diseases

The manifestations of the disease will differ depending on the degree of the disease, as well as the type of anemia.

Principles of treatment of anemia in premature babies:

Regardless of the type of anemia in premature babies, treatment is always long and complex. The choice of method for correcting the child's condition depends entirely on the type and degree of anemia.

Blood transfusion

This method of treating anemia in premature babies is used quite often in the first month after birth. As a rule, babies tolerate this procedure very well. Transfusion of blood or erythrocyte mass significantly improves the composition of red blood - increases the number of erythrocytes and hemoglobin. In most cases, blood transfusions are prescribed when the hemoglobin level in a premature baby drops below 130 g / l in the first week of life, which is accompanied by serious respiratory disorders, as well as the functioning of the heart and central nervous system. The main dangers and side effects of blood transfusions are:

The risk of contracting diseases such as HIV, cytomegalovirus infection, etc.
rejection of foreign blood
electrolyte imbalance in the blood
excess in the vascular bed of fluid that comes with the injected blood

Iron preparations

In premature babies, the most common form of anemia after two months of age is iron deficiency. The main drugs used to treat such children are iron preparations.

Important! How less weight child, the earlier treatment should be started. Doses of the drug should be larger.

Iron preparations for children are prescribed orally at a dosage of 5-7 mg per 1 kilogram of body weight per day between meals until the level of hemoglobin in the blood normalizes. In the future, for 1.5-2 months, they take an iron preparation in a half dose. For about 2 years, planned prevention of anemia of prematurity is carried out by means that the doctor will select. Increases the effectiveness of the use of iron preparations with ascorbic acid and vitamin E. At a hemoglobin level of 100 g / l and above, iron preparations are not used.

Important! Iron supplements should not be taken with milk!

Iron preparations in the form of injections are prescribed only in the following cases:

Intolerance to iron preparations
disorders in the stomach and intestines

The main side effects of iron supplements:

Stomach ache
constipation
diarrhea
nausea
painful injections

Treatment different type anemia is complex, which requires the appointment of different groups medicines. To this end, the pharmaceutical industry produces combined products that contain iron with folic acid, vitamin B12 and other vitamins.

Vitamins in the treatment of anemia

Most often, children with signs of anemia are prescribed B vitamins, especially B12, as well as folic and ascorbic acid, fish oil. All these substances increase the absorption of iron, improve the metabolism in the child's body, and participate in the synthesis of hemoglobin.

Diet therapy in the treatment of anemia

For newborn babies, the only food is mother's milk or adapted milk formula. Therefore, a qualitative improvement in the composition of food for children suffering from anemia lies in the fact that the necessary and valuable vitamins, proteins and trace elements (iron) are introduced additionally. Such therapy is carried out first in the conditions of the department for newborns strictly for medical reasons, in accordance with the body weight of the child and the degree of anemia. As the child grows older, he is assigned early introduction complementary foods rich in vitamins, minerals, trace elements and proteins. These substances are indispensable in the process of synthesis of red blood cells and the formation of hemoglobin in the blood of a growing organism.

Important! Anemia cannot be cured with diet alone. As well as taking medications without normalizing nutrition, often does not have the desired effect. Only an integrated approach to the problem of anemia in premature babies gives a lasting result.

Prevention of anemia in premature babies:

Effective preventive measures are as follows:

Appointment to pregnant women in the 2nd and 3rd trimester of iron preparations or vitamin complexes containing iron

The use of iron supplements by nursing mothers

From the age of three months, children born prematurely are prescribed iron supplements at a dose of 2 mg / kg per day. The minimum duration of admission is 3 months

For two years, and sometimes longer, control of blood counts once a quarter

Control over the diet of pregnant and lactating women. It is important to ensure that the menu contains foods rich in iron.

Prescribing fish oil preparations to children

The prognosis of anemia in premature babies is favorable. Means and methods modern medicine disease is successfully treated. Balanced diet, taking medicines and regular monitoring of blood counts are components of your child's health.

E.S.Sakharova, E.S.Keshishyan, CONSILIUM Medicum 2002, Appendix: Pediatrics

Anemia is one of the most common pathologies in young children. About 20% of full-term children suffer from this disease, and among premature babies in the first year of life, almost everyone develops anemia. At the same time, the severity of anemia is the higher, the lower the gestational age of the child. In the first months of life in premature babies with very low birth weight (less than 1500 g) and a gestational age of less than 30 weeks. severe anemia requiring red blood cell transfusion is up to 90%.
In the pathogenesis of early anemia of prematurity, not only the formation of iron deficiency, which is characteristic of all young children, but also factors of incomplete ontogenesis play a role.
Hematopoiesis in the prenatal period begins very early. Already in the first 2 weeks. development of the embryo, islets of hematopoiesis are determined - erythrocytes are produced yolk sac. Starting from 12-16 weeks, the main place of hematopoiesis becomes the liver and, to a lesser extent, the spleen. Approximately at 20 weeks. prenatal development the fetus begins erythropoiesis in the bone marrow, and gradually fades in the liver and spleen. Thus, by the time of birth in full-term children, hematopoiesis in the liver almost completely stops, while in very preterm infants, hematopoietic foci remain almost until the 40th week of gestation (i.e., from 3 weeks to 3 months of their actual age). In the early stages of intrauterine development, a small amount of erythrocytes. Before the onset of bone marrow hematopoiesis, the concentration of erythrocytes in the blood of the fetus grows slowly, and by the time of birth it increases sharply and is already 5-6 million per 1 mm 3.
Premature babies are characterized by morphological changes in erythrocytes. So, erythrocytes of an abnormal form make up 27%, while in full-term newborns it is only 14%. This contributes to the fact that the period of life of an erythrocyte in full-term infants is almost 2 times longer than in premature infants, and is 60-70 and 35-50 days, respectively.
Shortening the life of erythrocytes can contribute to the structural features of their membranes. When studying the composition of total lipids of erythrocyte membranes in children with early anemia of prematurity, it was found that from the 2nd week they have a decrease in the content of phospholipids and an increase in cholesterol. These changes progress to the 6th week of life and reach a maximum at the height of anemia, which correlates with clinical and laboratory symptoms.
In violation of the permeability of erythrocyte membranes in premature infants, a low level of vitamin E also plays a role, which is localized in the membranes and actively participates in peroxide phosphorylation. Vitamin E deficiency is observed in 86% of premature babies.
The fetal erythrocytes early stages ontogeny produce the germinal (embryonic) form of hemoglobin.
Between 7-12 weeks of intrauterine life, fetal hemoglobin is replaced by fetal hemoglobin. The hemoglobin level also depends on the gestational age, averaging 90 g/l at the 10th week, and 170±20 g/l by the 38th week.
Fetal hemoglobin has a higher affinity for oxygen and a slower release of oxygen to tissues compared to adult hemoglobin. Switching the synthesis of fetal hemoglobin to adult hemoglobin is under the control of genes located on the 11th and 16th chromosomes and begins at the 30th-32nd week of intrauterine development. The content of fetal hemoglobin in premature babies at birth averages 70-80%, in full-term newborns - 60-70%. More than half of the volume of fetal hemoglobin is replaced by adult hemoglobin in the first days of a child's life, then this process slows down somewhat, but by the 4-5th month of postnatal life, most children have about 1% of fetal hemoglobin. In premature babies, this process is slowed down, the main volume of hemoglobin change falls on the 40th week of gestation, and a complete change stretches for almost the entire first year of life. In addition, the delay in switching synthesis from fetal hemoglobin to adult hemoglobin is enhanced by severe hypoxia and fetal stress.
The hematocrit level is determined by the concentration of hemoglobin and red blood cells in the blood. Normally, the hematocrit in newborns is higher than in adults, and is 50-55%.
A reflection of the state of erythropoiesis is the level of reticulocytes. The average number of reticulocytes in a newborn is 4.2-7.2%. At the end of the 1st week of postnatal age, this figure decreases to the level of adults and is 1%.
At the birth of a full-term baby, a high hemoglobin content is determined, which, under conditions of increased oxygen consumption compared to intrauterine oxygen consumption, is excessive. This, in turn, leads to an increase in the production of erythropoietin and a decrease in erythropoiesis. With suppression of bone marrow function and increased destruction of erythrocytes, there is a gradual decrease and change in hemoglobin, which reaches 110-120 g / l in full-term children by the 8-12th week. If hemoglobin decreases to this threshold - for full-term 100-110 g / l, oxygen delivery to tissues is disturbed, which stimulates the production of erythropoietin. As a result, the process of increasing the production of erythrocytes begins.
In premature babies, the process of destruction of erythrocytes is faster due to the shorter period of life of these cells. The level of hemoglobin, at which the production of erythropoietin begins to increase in premature babies, is significantly lower than in full-term babies, and is 90-70 g / l (thus, such a hemoglobin level - critical for full-term babies, is acceptable for premature babies!).
In adults and older children, in response to even mild hypoxia, there is a rapid increase in the production of erythropoietin, while preterm infants are not able to produce adequate amounts of erythropoietin even with critical values circulating erythrocytes, which is due, apparently, to a lower oxygen demand.
Thus, anemia of prematurity is characterized by a progressive decrease in hemoglobin levels (up to 90-70 g / l and below), relative to low level reticulocytes and inhibition of bone marrow hematopoiesis.
Allocate early and late anemia of prematurity.
Early anemia develops on the 4th-10th week of postnatal life and is characterized by a decrease in the level of reticulocytes of less than 1%, the level of hemoglobin to 80-70 g/l and below, and the hematocrit to 20-30%.
The clinical picture of early anemia of prematurity is manifested by symptoms characteristic of true anemia, such as pallor of the skin, tachycardia or bradycardia, tachypnea, and apnea.
Among the causes of early anemia of prematurity, in addition to those indicated, a certain importance is attached to a high rate of increase in body weight and volume of circulating blood, incommensurable with the level of erythropoiesis.
In addition, the deficiency of folic acid, vitamin B6, microelements: zinc, copper, selenium, molybdenum plays a role in the genesis of early anemia of prematurity. Stocks of folic acid are depleted during the first weeks of life, which leads to a violation of the synthesis of folate by the intestinal microflora.
It is known that early anemia of prematurity can be one of the manifestations of infection and be potentiated by its postnatal development.
There are studies proving the relationship between the concentration of hemoglobin and the level of thyroid hormones (T3 and T4). Under conditions of a relative deficiency of T3 and T4, characteristic of premature babies, there is a violation of those stages of erythropoiesis that require intensive synthesis of specific proteins - enzymes involved in the formation of hemoglobin.
In addition to the "conditionally physiological" causes of anemia associated with incomplete ontogenesis, unfortunately, so-called iatrogenic causes play a certain role in potentiating the severity of anemia, such as frequent, albeit small in volume, blood loss as a result of blood sampling for laboratory research without replenishment of the BCC. According to the literature, during the first week of life, about 38.9 ml of blood is taken from a newborn premature baby for research. Relative to the total blood volume (80 ml/kg of weight), this is a very large figure.
Summarizing all that has been said, a combination of several factors play a role in the pathogenesis of anemia of prematurity:
a) shortened life span of erythrocytes;
b) prolonged circulation and late change of fetal hemoglobin;
c) the peculiarity of the metabolism of proteins, vitamins, microelements;
d) infectious agents, in particular gram-negative flora, for the vital activity of which an active consumption of iron is necessary;
e) iatrogenic causes.
One of the main methods of treatment of early anemia of prematurity is still blood transfusions. The most commonly used blood transfusions are donated red blood cells. Indications for red blood cell transfusions in case of anemia of prematurity are: decrease in hemoglobin below 130 g/l and hemotocrit below 0.4 in the period early adaptation(first 7 days of life) in combination with severe respiratory and cardiac disorders. The widespread use of blood transfusions in premature infants is associated with a low but significant risk. First of all, this is the possibility of transmission of viral infections (HIV, CMV) with transfusions, it is also possible to overload the vascular bed with fluid, the development of the "graft-versus-host" state, and electrolyte imbalance. Currently, alternative ways of solving this problem are being searched. One of them is the use of recombinant human erythropoietin, the effectiveness of which is now being intensively studied.
Late anemia of prematurity develops at the 3-4th month of life. It is more similar to iron deficiency anemia in young children. The clinical picture of late anemia of prematurity is characterized by decreased appetite, flattening of the weight curve, pale skin and mucous membranes, dry skin, enlarged liver and spleen. There is a decrease in serum iron - hypochromia, with a tendency to microcytosis and a hyperregenerative reaction of the bone marrow.
In addition to all the features inherent in early anemia of prematurity, during the development of late anemia, symptoms of iron deficiency begin to appear. The most active intake of iron from mother to fetus is carried out in the last 2 months. pregnancy, so prematurity at 4-8 weeks. can lead to a reduction in iron stores by 1.5-3 times compared with full-term.
In full-term babies, the reticuloendothelial system has a 15-20 day supply of iron. As soon as the lower level of hemoglobin is reached - 100-110 g / l in full-term and 70-90 g / l in premature, stimulation of erythropoiesis begins. If iron stores are insufficient, there is a further decrease in hemoglobin and anemia becomes iron-deficient. In a premature baby, the need for iron is higher than in a full-term baby, and there are strikingly fewer reserves. Given that iron is found in the body not only in the form of heme, but also goes to the construction of myoglobin and enzymes - catalase, peroxidase, cytochromes and cytochrome oxidase, its postnatal consumption is extremely high.
After birth, sources of iron for developing organism are the intake of exogenous iron in the composition food products and its utilization from endogenous reserves.
Attempts to enrich the diet with the introduction of adapted mixtures, including those enriched with iron, do not lead to the desired result, since the latter is poorly absorbed. For premature babies, especially in the first months of life, the only physiological food product that ensures the balance of iron metabolism in the body is mother's milk, balanced in all ingredients in accordance with the physiological needs of the growing body. Although in human milk the iron content is low (0.2-1.5 mg / l), there are special mechanisms for more efficient absorption (up to 50%). However, big problem is the maintenance of lactation in women who are under stress as a result of prematurely terminated pregnancy and a sick child. educational work, psychological support mothers are the only way to provide breastfeeding premature baby.
For the dietary correction of iron deficiency, timely (but not earlier than the 4-5th month of life) introduction of complementary foods (fruits, vegetables, later, after 8 months - meat) is required. At the same time, studies have shown that for the treatment of anemia (but not for its prevention), it is not enough just to increase the level of dietary iron, but a drug subsidy is required.
Why is iron deficiency anemia so dangerous?
Iron deficiency anemia contributes to the development chronic hypoxia, which in turn can lead to a slowdown in the mental and psychomotor development of the child.
In this regard, the treatment of anemia in preterm infants and the prevention of iron deficiency in all children is important and mandatory. integral part in the general scheme for monitoring children in the 1st year of life. In addition to important dietary approaches, the early administration of prophylactic doses of iron preparations to all premature babies is relevant. The drugs of choice in this case are modern representatives of the hydroxide polymaltose complex of ferric iron: Maltofer and Ferrum Lek. Hydroxide polymaltose complex is stable under physiological conditions, which excludes the formation of free iron ions. Unlike the previously common salt (ionic) iron preparations - divalent compounds of iron salts (for example, ferrous sulfate), polymaltose complexes (Maltofer and Ferrum Lek) do not irritant on the intestinal mucosa, which often manifests itself in the form of constipation, diarrhea, nausea, regurgitation. The absorption of iron from polymaltose complexes is close to the absorption of heme iron and is provided by an active transport mechanism, the most physiological for the body. In this case, iron is directly transferred through transferrin receptors to hematopoietic sites or delivered to iron storage sites, where it is deposited in the reticuloendothelial system (liver and spleen) in the form of ferritin.
Clinical studies of the drug "Maltofer" showed its equal effectiveness in comparison with salt preparations. At the same time, the number of side effects from gastrointestinal tract 3 times less with the use of the iron polymaltose complex, and the number of patients who refused to continue the course of treatment is more than 2 times more in the group of salt preparations.
The chemical structure of the complex does not release free iron. Together with the active transport mechanism of iron absorption, this protects the body from intoxication with free iron ions, as well as their oxidative effects, inherent in iron salt preparations.
The same mechanisms support the self-regulation system on the principle of "feedback": the absorption of iron from the complex stops as soon as its required level in the body is restored, which eliminates the possibility of poisoning with these drugs in case of their overdose.
Premature infants from the first weeks of life up to the 1st year are recommended to take these iron preparations prophylactically at the rate of 2 mg/kg/day of elemental iron. The therapeutic dose is 5 mg / kg / day of elemental iron and does not change until the hemoglobin level normalizes. Monitoring of red blood parameters (hemoglobin level, CP, erythrocytes) in premature babies after discharge from the nursing departments must be carried out without fail at 3, 6 and 12 months, then 2 times a year, and if anemia is detected, every 14 days until the hemogram indicators stabilize .
Taking into account the peculiarities of the pathogenesis of anemia in premature infants, the tendency to develop a hyporegenerative reaction of the bone marrow, megaloblastosis, macrocytosis, increased hemolysis of erythrocytes, children with low birth weight at birth need early, from 7 days of life, the introduction of folic acid 1 mg per day, vitamin E 20 mg/kg per day, B vitamins.
According to the Order of the Ministry of Health of the Russian Federation No. 375 dated 12/18/97 on preventive vaccinations, iron deficiency anemia is not a contraindication to vaccination. On the other hand, premature babies are special group risk for the development of a complicated infectious process. Therefore, even in the case of severe manifestations of anemia, preventive vaccinations can be carried out immediately after the relief of acute manifestations. A moderate decrease in hemoglobin, antianemic treatment is not a reason to postpone vaccination.

Literature

1. Bisyarina V.P., Kazakova L.M. Iron deficiency anemia in young children. M., 1979; 176.
2. Nex E., Cristensen N.S., Olesen S. Volume of blood removed for analytical purposes during hospitalization of low birth weight infants. Clinical chemistry, 1981; 27:759-61.
3. Aldysheva T.V. The combination of substances in blood plasma and the activity of antioxidant enzymes in erythrocytes in the presence of anemia in premature babies. Issues of adaptation of premature babies and children infancy. M., 1985; 127-30
4. Degtyarev D.N., Kurmasheva N.A., Volodin N.N. Modern ideas about the pathogenesis and treatment of anemia in premature babies. Lectures of the department of neonatology of the Russian State Medical University, 1994.
5. Dallmann P.R. Nutritional anemia in infancy in Tsang R.C., Nicols B.L. Nutrition during infancy, Philadelphia, 1988.
6. Krasnitskaya L.N. The content of thyroid hormones, testosterone and cortisol in the blood serum of premature infants with early anemia. Abstract diss. Candidate of Medical Sciences, L., 1988; 22.
7. Prigogina T.A. The effectiveness of recombinant erythropoietin in the complex prevention and treatment of early anemia of prematurity. Diss. Candidate of Medical Sciences, M., 1988.
8. Akre D. Feeding children of the first year of life: functional bases. WHO Bulletin, 1989; appendix to volume 67: 30-35.
9. Walter T. Infancy: mental and motor development. American Journal of Clinical Nutrition, 1989; 50:655-66
10. Jacobs P. et. al. Better tolerance of iron polymaltose complex compared with ferrous sulfate in the treatment of anemia. Hematology, 2000; 5:77-83
11. Geisser P. et. al. Structure / histotoxicity relationship of oral iron preparations. Drug Research, 1992; 42:1439-52.
12. Tuomainen, T-P, et al. Oral supplementation with ferrous sulfate but not with non-ionic iron polymaltose complex increases the susceptibility of plasma lipoproteins to oxidation, Nutrition Research, 1999; 19:1121-32
13. Geisser P., Hohl H. and Mueller A. Klinische Wirksamkeit dreier verschiedener Eisenpraeparate an Schwangeren. Switzerland. Apotheker-Zeitung, 1987; 14:393-8
14. Fedorov A.M. About the new calendar of preventive vaccinations. children's doctor, 1999; 1: 27-9.

Anemia in premature babies.

Anemia is one of the most common pathologies in young children. About 20% of full-term children suffer from this disease, and among premature babies in the first year of life, almost everyone develops anemia. At the same time, the severity of anemia is the higher, the lower the gestational age of the child. In the first months of life in premature babies with very low birth weight (less than 1500 g) and a gestational age of less than 30 weeks. severe anemia requiring red blood cell transfusion is up to 90%.

In the pathogenesis of early anemia of prematurity, not only the formation of iron deficiency, which is characteristic of all young children, but also factors of incomplete ontogenesis play a role.

Hematopoiesis in the prenatal period begins very early. Already in the first 2 weeks. development of the embryo, islets of hematopoiesis are determined - erythrocytes are produced by the yolk sac. Starting from 12-16 weeks, the main place of hematopoiesis becomes the liver and, to a lesser extent, the spleen. Approximately at 20 weeks. intrauterine development of the fetus, erythropoiesis begins in the bone marrow, and gradually fades in the liver and spleen. Thus, by the time of birth in full-term children, hematopoiesis in the liver almost completely stops, while in very preterm infants, hematopoietic foci remain almost until the 40th week of gestation (i.e., from 3 weeks to 3 months of their actual age). In the early stages of intrauterine development, a small amount of red blood cells is noted. Before the onset of bone marrow hematopoiesis, the concentration of erythrocytes in the blood of the fetus grows slowly, and by the time of birth it increases sharply and is already 5–6 million per 1 mm3.

Premature babies are characterized by morphological changes in erythrocytes. So, erythrocytes of an abnormal form make up 27%, while in full-term newborns it is only 14%. This contributes to the fact that the period of life of an erythrocyte in full-term infants is almost 2 times longer than in premature infants, and is 60–70 and 35–50 days, respectively.

Shortening the life of erythrocytes can contribute to the structural features of their membranes. When studying the composition of total lipids of erythrocyte membranes in children with early anemia of prematurity, it was found that from the 2nd week they have a decrease in the content of phospholipids and an increase in cholesterol. These changes progress to the 6th week of life and reach a maximum at the height of anemia, which correlates with clinical and laboratory symptoms.

In violation of the permeability of erythrocyte membranes in premature infants, a low level of vitamin E also plays a role, which is localized in the membranes and actively participates in peroxide phosphorylation. Vitamin E deficiency is observed in 86% of premature babies.
Germinal erythrocytes in the early stages of ontogenesis produce the germinal (embryonic) form of hemoglobin.

Between 7–12 weeks of intrauterine life, fetal hemoglobin is replaced by fetal hemoglobin. The hemoglobin level also depends on the gestational age, averaging 90 g/l at the 10th week, and 170±20 g/l by the 38th week.

Fetal hemoglobin has a higher affinity for oxygen and a slower release of oxygen to tissues compared to adult hemoglobin. Switching the synthesis of fetal hemoglobin to adult hemoglobin is controlled by genes located on chromosomes 11 and 16 and begins at 30–32 weeks of fetal development. The content of fetal hemoglobin in premature babies at birth averages 70-80%, in full-term newborns - 60-70%. More than half of the volume of fetal hemoglobin is replaced by adult hemoglobin in the first days of a child's life, then this process slows down somewhat, but by the 4–5th month of postnatal life, most children have about 1% of fetal hemoglobin. In premature babies, this process is slowed down, the main volume of hemoglobin change falls on the 40th week of gestation, and a complete change stretches for almost the entire first year of life. In addition, the delay in switching synthesis from fetal hemoglobin to adult hemoglobin is enhanced by severe hypoxia and fetal stress.

The hematocrit level is determined by the concentration of hemoglobin and red blood cells in the blood. Normally, the hematocrit in newborns is higher than in adults, and is 50-55%.

A reflection of the state of erythropoiesis is the level of reticulocytes. The average number of reticulocytes in a newborn is 4.2–7.2%. At the end of the 1st week of postnatal age, this figure decreases to the level of adults and is 1%.

At the birth of a full-term baby, a high hemoglobin content is determined, which, under conditions of increased oxygen consumption compared to intrauterine oxygen consumption, is excessive. This, in turn, leads to an increase in the production of erythropoietin and a decrease in erythropoiesis. With suppression of bone marrow function and increased destruction of erythrocytes, there is a gradual decrease and change in hemoglobin, which reaches 110–120 g/l by the 8–12th week in full-term children. If hemoglobin drops to this threshold - for full-term 100-110 g / l, oxygen delivery to tissues is impaired, which stimulates the production of erythropoietin. As a result, the process of increasing the production of red blood cells begins.

In premature babies, the process of destruction of erythrocytes is faster due to the shorter period of life of these cells. The level of hemoglobin, at which the production of erythropoietin begins to increase in premature babies, is significantly lower than in full-term babies, and is 90–70 g/l (thus, such a hemoglobin level, which is critical for full-term babies, is acceptable for premature babies!).

In adults and older children, in response to even mild hypoxia, a rapid increase in erythropoietin production is observed, while preterm infants are not able to produce adequate amounts of erythropoietin even at critical values ​​​​of circulating erythrocytes, which is apparently due to a lower oxygen demand.

Thus, anemia of prematurity is characterized by a progressive decrease in the level of hemoglobin (up to 90–70 g/l and below), a relatively low level of reticulocytes, and inhibition of bone marrow hematopoiesis.

Allocate early and late anemia of prematurity.

Early anemia develops on the 4th–10th week of postnatal life and is characterized by a decrease in the level of reticulocytes to less than 1%, the level of hemoglobin to 80–70 g/l and below, and the hematocrit to 20–30%.

The clinical picture of early anemia of prematurity is manifested by symptoms characteristic of true anemia, such as pallor of the skin, tachycardia or bradycardia, tachypnea, and apnea.

Among the causes of early anemia of prematurity, in addition to those indicated, a certain importance is attached to a high rate of increase in body weight and volume of circulating blood, incommensurable with the level of erythropoiesis.

In addition, the deficiency of folic acid, vitamin B6, microelements: zinc, copper, selenium, molybdenum plays a role in the genesis of early anemia of prematurity. Stocks of folic acid are depleted during the first weeks of life, which leads to a violation of the synthesis of folate by the intestinal microflora.
It is known that early anemia of prematurity can be one of the manifestations of infection and be potentiated by its postnatal development.
There are studies proving the relationship between the concentration of hemoglobin and the level of thyroid hormones (T3 and T4). In conditions of relative deficiency of T3 and T4, which is characteristic of premature babies, there is a violation of those stages of erythropoiesis that require intensive synthesis of specific proteins - enzymes involved in the formation of hemoglobin.

In addition to the "conditionally physiological" causes of anemia associated with incomplete ontogenesis, unfortunately, so-called iatrogenic causes play a certain role in potentiating the severity of anemia, such as frequent, albeit small in volume, blood loss as a result of blood sampling for laboratory studies without replenishing the BCC. According to the literature, during the first week of life, about 38.9 ml of blood is taken from a newborn premature baby for research. Relative to the total blood volume (80 ml/kg of weight), this is a very large figure.

Summarizing all that has been said, a combination of several factors play a role in the pathogenesis of anemia of prematurity:

A) shortened lifespan of erythrocytes;
b) prolonged circulation and late change of fetal hemoglobin;
c) the peculiarity of the metabolism of proteins, vitamins, microelements;
d) infectious agents, in particular gram-negative flora, for the vital activity of which an active consumption of iron is necessary;
e) iatrogenic causes.

One of the main methods of treatment of early anemia of prematurity is still blood transfusions. The most commonly used blood transfusions are donated red blood cells. Indications for red blood cell transfusions in anemia of prematurity are: decrease in hemoglobin below 130 g/l and hemotocrit below 0.4 during early adaptation (the first 7 days of life) in combination with severe respiratory and cardiac disorders. The widespread use of blood transfusions in premature infants is associated with a low but significant risk. First of all, this is the possibility of transmission of viral infections (HIV, CMV) with transfusions, it is also possible to overload the vascular bed with fluid, the development of the "graft-versus-host" state, and electrolyte imbalance. Currently, alternative ways of solving this problem are being searched. One of them is the use of recombinant human erythropoietin, the effectiveness of which is now being intensively studied.

Late anemia of prematurity develops at the 3-4th month of life. It is more similar to iron deficiency anemia in young children. The clinical picture of late anemia of prematurity is characterized by decreased appetite, flattening of the weight curve, pale skin and mucous membranes, dry skin, enlarged liver and spleen. There is a decrease in serum iron - hypochromia, with a tendency to microcytosis and a hyperregenerative reaction of the bone marrow.

In addition to all the features inherent in early anemia of prematurity, during the development of late anemia, symptoms of iron deficiency begin to appear. The most active intake of iron from mother to fetus is carried out in the last 2 months. pregnancy, so prematurity at 4-8 weeks. can lead to a reduction in iron stores by 1.5-3 times compared with full-term.

In term infants, the reticuloendothelial system has a 15–20 day supply of iron. As soon as the lower level of hemoglobin is reached - 100-110 g / l in full-term and 70-90 g / l in premature, stimulation of erythropoiesis begins. If iron stores are insufficient, there is a further decrease in hemoglobin and anemia becomes iron-deficient. In a premature baby, the need for iron is higher than in a full-term baby, and there are strikingly fewer reserves. Considering that iron is found in the body not only in the form of heme, but also goes to the construction of myoglobin and enzymes - catalase, peroxidase, cytochromes and cytochrome oxidase, its postnatal consumption is extremely high.

After birth, the sources of iron for the developing organism are the intake of exogenous iron in the composition of food products and its utilization from endogenous reserves.

Attempts to enrich the diet with the introduction of adapted mixtures, including those enriched with iron, do not lead to the desired result, since the latter is poorly absorbed. For premature babies, especially in the first months of life, the only physiological food product that ensures the balance of iron metabolism in the body is mother's milk, balanced in all ingredients in accordance with the physiological needs of the growing body. Although the content of iron in human milk is low (0.2-1.5 mg / l), there are special mechanisms for more efficient absorption (up to 50%). At the same time, a big problem is the maintenance of lactation in women who are under stress as a result of prematurely terminated pregnancy and a sick child. Educational work, psychological support for the mother are the only way to provide breastfeeding for a premature baby.

For the dietary correction of iron deficiency, timely (but not earlier than the 4–5th month of life) introduction of complementary foods (fruits, vegetables, later, after 8 months - meat) is required. At the same time, studies have shown that for the treatment of anemia (but not for its prevention), it is not enough just to increase the level of dietary iron, but a drug subsidy is required.

Why is iron deficiency anemia so dangerous?

Iron deficiency anemia contributes to the development of chronic hypoxia, which in turn can lead to a slowdown in the mental and psychomotor development of the child.

In this regard, the treatment of anemia in premature infants and the prevention of iron deficiency in all children is an important and mandatory part of the overall scheme for monitoring children in the 1st year of life. In addition to important dietary approaches, the early administration of prophylactic doses of iron preparations to all premature babies is relevant. The drugs of choice in this case are modern representatives of the hydroxide polymaltose complex of ferric iron: Maltofer and Ferrum Lek. Hydroxide polymaltose complex is stable under physiological conditions, which excludes the formation of free iron ions. Unlike previously common salt (ionic) iron preparations - divalent compounds of iron salts (for example, ferrous sulfate), polymaltose complexes (Maltofer and Ferrum Lek) do not irritate the intestinal mucosa, which often manifests itself in the form of constipation, diarrhea, nausea , regurgitation. The absorption of iron from polymaltose complexes is close to the absorption of heme iron and is provided by an active transport mechanism, the most physiological for the body. In this case, iron is directly transferred through transferrin receptors to hematopoietic sites or delivered to iron storage sites, where it is deposited in the reticuloendothelial system (liver and spleen) in the form of ferritin.

Clinical studies of the drug "Maltofer" showed its equal effectiveness in comparison with salt preparations. At the same time, the number of side effects from the gastrointestinal tract is 3 times less with the use of the iron polymaltose complex, and the number of patients who refused to continue the course of treatment is more than 2 times more in the group of salt preparations.

The chemical structure of the complex does not release free iron. Together with the active transport mechanism of iron absorption, this protects the body from intoxication with free iron ions, as well as their oxidative effect, which is inherent in iron salt preparations.

The same mechanisms support the system of self-regulation on the principle of "feedback": the absorption of iron from the complex stops as soon as its required level in the body is restored, which eliminates the possibility of poisoning with these drugs in case of their overdose.

Premature infants from the first weeks of life up to the 1st year are recommended to take these iron preparations prophylactically at the rate of 2 mg/kg/day of elemental iron. The therapeutic dose is 5 mg / kg / day of elemental iron and does not change until the hemoglobin level normalizes. Monitoring of red blood parameters (hemoglobin level, CP, erythrocytes) in premature infants after discharge from the nursing departments must be carried out without fail at 3, 6 and 12 months, then 2 times a year, and if anemia is detected, every 14 days until the hemogram parameters stabilize .

Taking into account the peculiarities of the pathogenesis of anemia in premature infants, the tendency to develop a hyporegenerative reaction of the bone marrow, megaloblastosis, macrocytosis, increased hemolysis of erythrocytes, children with low birth weight at birth need early, from 7 days of life, the introduction of folic acid 1 mg per day, vitamin E 20 mg/kg per day, B vitamins.

According to the Order of the Ministry of Health of the Russian Federation No. 375 dated 12/18/97 on preventive vaccinations, iron deficiency anemia is not a contraindication to vaccination. On the contrary, premature babies represent a special risk group for the development of a complicated infectious process. Therefore, even in the case of severe manifestations of anemia, preventive vaccinations can be carried out immediately after the relief of acute manifestations. A moderate decrease in hemoglobin, antianemic treatment is not a reason for postponing vaccination.