Rickets in infants: symptoms and treatment. Rickets in the initial period, mild, acute

Lecture No. 9

Rickets is a general disease of a child, accompanied by metabolic disorders, significant disorders of bone formation and dysfunction of all organs and systems, immediate cause, which is most often hypovitaminosis D.

Rickets is caused by a temporary discrepancy between the needs of a growing organism for phosphorus and calcium and the insufficiency of the systems that ensure their delivery to the child’s body. Rickets has been known for a long time. First identified in 1650, by Kotovitsky in 1847. Filatov determined the significance in the pathology of young children. Rickets is not one of the dangerous diseases of young children, but, nevertheless, there is a high mortality rate

takes part because it directly exposes the child’s body to diseases and generally reduces its endurance and strength to resist harmful factors. People with rickets die from gastrointestinal diseases, pneumonia, severe forms they rarely have lungs, 60% of young children. Modern rickets occurs at an earlier age. Mild forms affect the development of the child because metabolism is disrupted, the body's resistance decreases, therefore, children suffer from rickets, more often in women who suffer concomitant diseases: pneumonia, bronchitis, gastrointestinal tract. These diseases have a protracted course and the development of complications. The main significance in the etiology of rickets is the insufficient intake of vitamins D, B, C, A, calcium salts, phosphorus, magnesium and others into the body, as well as a lack of proteins during the periods of intrauterine and postnatal development.

Rickets should be considered as a disease with a complex etiopathogenesis with exo- and endogenous components.

Endogenous background:

The high speed and remodeling of the skeleton characteristic of a growing organism, especially in the first years of life and due to this increased need in salts of calcium, phosphorus, vitamin D and others with relative weakness and imperfection of the systems ensuring their delivery and metabolism. Endogenous risk factors include young maternal age, frequent pregnancies and a short interval between them, abortions, low birth weight of the child, birth during multiple pregnancy, diseases of the skin, gastrointestinal tract, kidneys, immaturity of systems that provide transport of calcium, phosphorus and vitamin D salts, perinatal hypoxia, malnutrition, genetic predisposition, etc. From the outside placenta - a pathology leading to disruption of the formation of calcium-regulating hormones, placental peptide. These substances provide increased calcium pumping from the mother several weeks before birth in order to increase fetal bone density and create a calcium reserve. Premature babies born before this period are deficient in calcium and phosphorus and develop rickets.

Exogenous background

various food climatic and geographical features (with a harsh climate and reduced background insolation), mixed and artificial feeding (deficiency of proteins, amino acids, microelements, vitamins), social and living conditions (large family, twins, low material security), environmental background (habitat pollution) , hygienic background (poor care, infrequent nutrition).

Breastfed children can also get sick, but children on mixed or artificial feeding are more common if they are not introduced in a timely manner. food additives(excess carbohydrates because grain products contain phytic acid, which in compounds with calcium forms an insoluble complex that contributes to the disorder mineral metabolism. Children who have suffered a prenatal hypoxic condition, premature babies, and twins are also prone to rickets. insufficiency of calcium and vitamin D during intrauterine development, their need increases before birth because growth increases. Children with prenatal dystrophy, northern latitudes (reduced insolation), children of large cities (polluted water bodies), receiving long-term anticonvulsant therapy, with cystic fibrosis, thrombolytic diseases, liver and kidney diseases, are more seriously ill because Violations of vitamin D metabolism contribute to the occurrence of rickets: respiratory, gastrointestinal and other diseases, defects in care and education, and inadequate regimen motor activity, insufficient stay of the child on fresh air, unfavorable living conditions. ATP deficiency reaction - caused by cellular energy deficiency.

Congenital rickets occurs among children born to women with extragenital diseases and severe pregnancy pathologies.

Violation of phosphorus-calcium metabolism. Regulation of vitamin D by parathyroid, thyroid, pancreas, adrenal hormones, etc. Citric acid is more significant in calcium metabolism. Disturbances in the enzyme system of phosphorylase, phosphatase, and diastase are associated with the exchange of phosphorus and calcium. Alkaline phosphatase is involved in bone formation; normally, due to the stimulation of osteoblasts, osteoid tissue is formed, which after the deposition of phosphorus and calcium phosphate in it. With rickets, this process is disrupted.

There are 7 types of vitamin D in foods of plant and animal origin. The most active are D3 cholecalceferol (animal) and D2 ergocalceferol (vegetable).

Ways of getting vitamin D into the body:

2. formation in the skin under the influence of ultraviolet radiation (280-320 nm) of provitamin D7 (dehydrocholesterol), which is converted into vitamin D3. Vitamin D is found in liver, fish (cod), fish roe, egg yolk, butter, women's and cow's milk.

Daily requirement 100-400 IU.

1 liter of human milk 50-70 IU

1 liter of cow's milk 20-30 IU

In the bones there is osteoporosis and osteomalacia. The content of inorganic phosphorus remains reduced, since parathyroid hormone inhibits the reabsorption of phosphorus in the renal tubules, thus hyperphosphatemia is more early sign. For normal remodeling and growth of the skeleton, mobilization of calcium from the bone, 1,25-hydroxycalceferol is required; as vitamin D decreases, the level of this metabolite decreases, as a result of which the absorption of calcium in the intestine and its mobilization from the skeleton are impaired, hypocalcemia and hypomagnesemia develop. Since there is a lack of calcium, phosphorus, vitamin D, etc., the synthesis of the organic matrix of the bone, bone growth is impaired, and the functioning of the bone as an organ is impaired.

Causes of acidosis:

1. disturbance in the Krebs cycle with excess oxalic acid.

2.decreased magnesium content and hypocitremia

3.impaired reabsorption of phosphorus in the renal tubules because there is an excess of parathyroid hormone.

Acidosis in the body supports osteoporosis with osteomalacia. Disorders develop skeletal system, there are 3 types of disorders:

1. Osteomalacia - various manifestations, softness of large fontanelles, cranial sutures, ribs, curvature of the clavicles, forearms, changes in the length of the limbs.

2. Osteoid hyperplasia - enlargement of the frontal and parietal tubercles.

3. Osteogenesis disorders - late closure of fontanelles, teething, polyhypovitaminosis, especially C, which improves the absorption of vitamin D and is involved in bone formation. Deficiency of vitamins B7 and A - osteoporosis develops, protein metabolism is disrupted, vitamin D deficiency increases the excretion of amino acids in the urine, collagen structure is disrupted, carbohydrate and lipid metabolism, there is a decrease in blood citric acid.

Classification of rickets

1. Timing of occurrence

Congenital

Acquired

2. According to the leading pathogenetic factor

Exogenous

Endogenous

Mixed

3. By period

Elementary

High period

Convalescence period

Period of residual effects.

4. By severity

1st degree easy

2nd degree average

3rd degree severe

5. By the nature of the flow

Subacute

Chronic (recurrent)

6. Depending on the predominant deficiency

Calciphenic

Phosphoropenic

With a slight disturbance of phosphorus metabolism.

Exogenous rickets include vitamin D-mediated rickets, nutritional rickets, and iatrogenic rickets.

Endogenous reactions include reactions during hypoxic therapy, reactions caused by immaturity..., rickets caused by impaired absorption due to enterococcosis.

Clinic

Initial period

Changes in the autonomic nervous system develop, at 4-5 weeks, more often at 3 months, in premature infants, from 2-3 weeks anxiety, shuddering in sleep, excessive sweating during feeding and during sleep, increased irritability skin, the child rubs his head on the pillow - bald patches on the back of his head. Increased alkaline phosphatase activity, increased urinary excretion of ammonia, phosphorus, fatty acids, calcium is normal. All this precedes changes in the bones; they appear at the end of the initial period - softening of the large fontanel and cranial sutures. The duration of the period is from 2-3 weeks to 2-3 months. If not eliminated etiological factor the disease moves into the next stage.

High period

Further progression of the disease, bone manifestations increase. The rachitic process affects all bones of the skeleton; changes are more pronounced in those bones that grow more rapidly. Based on bone changes, one can judge the time of onset of the disease - first of all, they appear in the skull, first only the softness of the edges of the fontanelles, sutures, softening of the flat bones of the skull; in severe cases, they spread to all the bones of the skeleton and the base of the skull. The softness of the bones of the skull leads to its deformation, the back of the head flattens on the lying side, and asymmetry of the head occurs. Due to the excessive formation of osteoid tissue, the frontal and parietal tubercles protrude, as a result of which the head becomes square shape, sunken bridge of the nose, “Olympic” forehead, exophthalmos. Changes in the dental system: violation of the time and order of teeth eruption, enamel defects resulting in the development of caries, malocclusion, gothic palate, all these signs develop if rickets develops for the first time 3 months of life. If rickets develops later than 3 months of life, there are often changes in the chest because increased formation of osteoid tissue, thickening occurs at the border of the bone and cartilage joints, the so-called “rachitic rosary” (ribs 5-8), increased curvature of the clavicles, the chest is compressed from the sides, the lower aperture is enlarged, and according to the line of attachment of the diaphragm, Galliso’s line is formed. In severe cases, the anterior part of the chest protrudes forward (keel-shaped “chicken” chest) changes in the spine: when the child sits in the lumbar region, kyphosis (hunchback), and when walking - lordosis, scoliosis. The described changes develop if rickets occurs between 3 and 6 months of a child’s life. After 6 months, deformities appear tubular bones, there is thickening of the epiphyses of the bones of the forearm, legs, phalanges, curvature of the bones of the lower extremities in the form of the letter “O” or “X”, flat feet, flat rachitic pelvis. Rickets is not limited to bone damage; the nervous and muscular systems suffer.

Nervous system: in the process of disturbances of the Krebs cycle, a deficiency of carboxylase develops, resulting in insufficient formation of acetylcholine, which, along with a decrease in calcium levels, leads to increased nervous excitability. A lack of acetylcholine leads to disruption of nerve impulse transmission - muscle hypotension develops. Myotonia is also associated with a decrease in phosphorus in the blood, due to muscle hypotonia and smooth muscle intestines, a spread out “frog” stomach appears, divergence of the rectus abdominis muscles. Static and motor function is delayed, therefore, children later hold their head, sit, stand, and walk. With rickets, the functions of the liver, endocrine glands are impaired. In children with rickets, the respiratory function pulmonary tissue, the chest is deformed, hypotension of the diaphragm develops, functional and morphological changes lung tissue. The lungs along the spine have atelectatic areas, which contributes to the development of pneumonia. Shortness of breath appears, heart function worsens: tachycardia, muffled sounds, systolic murmur is heard. The ECG shows metabolic disturbances, signs of hypocalcemia - an increase in the Q and T waves, a shortening of the T wave. Weakness in the contraction of the diaphragm - stagnation of blood in the liver - enlargement of the liver. Stagnation develops in the system portal vein, enlarged spleen, deficiency of vitamins A, B1, B5, B6, E, magnesium, calcium, phosphorus, zinc, disturbance of mineral and protein metabolism, increased alkaline phosphatase activity, with a slight decrease in calcium levels, citric acid content decreases, phosphate excretion increases, ammonia, amino acids.

In patients of 2.3 degrees, hypochromic anemia develops, the cause of which is a decrease in amino acids, iron, vitamins, changes in the structure and function of erythrocyte membranes, acidosis (hemolysis).

The peak period lasts from 8 weeks to 8 months.

Convalescence period

Characterized by reverse development symptoms, changes in the nervous system disappear, the edges of large fontanelles and sutures become denser, craniotabes decreases or disappears, teeth appear, static functions are restored, anemia, muscle hypotension decreases or disappears. Mobilization of calcium from the blood and its deposition into bones. The child may have spasmophilia.

Period of residual effects

At 2-3 years of age, after rickets of 2-3 degrees of severity, children have bone deformations, enlarged liver and spleen, and anemia.

1st degree of severity - not a large number of mild signs of rickets from the autonomic nervous system: sweating, anxiety, baldness of the back of the head, softening of the edges of the fontanelles, sutures, flattening of the back of the head, mild rachitic rosary, sometimes muscle hypotonia, no residual effects. No more than 2-3 systems are affected (autonomic, skeletal, muscular).

2nd degree - 5 systems are affected, aggravating changes in the nervous system, bone, muscle, hematopoietic enlargement of the liver, spleen, dysfunction of internal organs. Damage to bones in at least 2-3 parts of the skeleton.

From the outside muscular system– hypotension, divergence of the rectus abdominis muscles, “frog belly”, impaired static function. Changes in the blood - mild anemia, in full-term infants no earlier than 4-5 months, in premature infants earlier.

3rd degree of severity: pronounced changes in the nervous system, lethargy, motor function is not developed or lost, muscle hypotonia, loose joints, deformation of the skull, chest, limbs, enlarged liver, spleen. Functional disorders of cardio-vascular system, expansion of the borders of the heart, tachycardia, violation heart rate, functional breathing disorders, shortness of breath, atelectasis, hypoxemia. Not earlier than 6-7 months from the onset of the disease.

Acute - in the first half of the year, especially in premature and rapidly gaining weight children. It is characterized by a rapid increase in symptoms, pronounced disorders of the central nervous system, the process of bone softening prevails over the process of osteoid hyperplasia. In a biochemical blood test - a decrease in phosphorus, an increase in alkaline phosphatase activity.

Subacute – slow development of the disease: osteoid hyperplasia (enlargement of the frontal and parietal tubercles), rachitic rosary, enlargement of tubular bones, muscle hypotonia, anemia. In children with malnutrition, rickets develops in the second half of the year. If the child received vitamin D as a prophylaxis, then the dose is not sufficient. Under the influence of treatment, the acute stage passes into the subacute stage. After intercurrent illnesses subacute stage can turn into an acute - recurrent course, a change in deterioration and exacerbation, which is associated with changes in living conditions, the environment in an unfavorable direction, repeated diseases, poor nutrition, deficiency associated with water, insolation. Clinically it can be suspected based on the existing changes various departments skeleton. To confirm the diagnosis - an x-ray of the forearm. On the radiograph, stripes correspond to zones of calcification (in case of relapses) formation in the metaphyses. The number of exacerbations is determined by the number of these zones.

Form from predominant deficiency

1. Calcium deficiency (calcipenic variant) bone deformation, osteomalacia predominates, increased neuromuscular excitability, tremors of the extremities, disturbance of day and night sleep, unmotivated anxiety, changes in the autonomic nervous system, increased sweating, tachycardia, decreased calcium in serum and erythrocytes.

2. Phosphorus deficiency (phosphoropenic variant) symptoms are more pronounced, lethargy, muscle hypotonia, rosary beads, bracelets, enlargement of the frontal and parietal tubercles, weakness of the ligamentous-articular apparatus, “frog” stomach, decreased phosphorus in the blood.

3. With minimal disturbances of mineral metabolism, subacute course, moderate hyperplasia of osteoid tissue in the area of ​​the tuberosities and the absence of clear changes in the nervous and muscular systems.

CONGENITAL RICHITIS

During the newborn period - extensive foci of osteomalacia, rachitic rosary, softness and pliability of the chest bones during palpation, non-closure of the large and small fontanel. The large fontanelle is widened, the divergence of cranial sutures, nonspecific manifestations of hypocalcemia: tremor, tachycardia, increased neuromuscular excitability.

IATROGENIC RICHITIS

Occurs as a result of taking anticonvulsants(treatment perinatal encephalopathy). Phenobarbital aggravates hypocalcemia - convulsive syndrome develops - the dose of phenobarbital is increased. Appears at 2-3 weeks of treatment with phenobarbital, changes in the central nervous system, poor cardiac excitability, sharp cry, tremors, convulsive readiness, enlargement of the frontal and parietal tubercles, rosary beads on the ribs. It is distinguished by a progressive increase in bone manifestations during phenobarbital therapy, there is no effect from usual doses vitamin D.

TREATMENT

Treatment should be comprehensive, systematic, long-term, aimed at eliminating the causes of rickets, eliminating vitamin D deficiency (and others).

Specific: UV irradiation, vitamin D.

Nonspecific: (not always hypovitaminosis D) replenish phosphorus, calcium, proteins, etc. Long stay in the fresh air, diet in accordance with age, timely introduction of food additives and complementary foods.

To correct polyhypovitaminosis, take multivitamins once a day, every other day. If the child is on artificial or mixed feeding and receive adapted mixtures containing essential vitamins he does not need to take multivitamins.

Vitamin D strictly according to indications: biochemical analysis, craniotabes, hypocalcemia, hypophosphatemia, increased alkaline phosphatase, etc.

The peak period: vitamin D 2000-5000 IU/day course 30-45 days, after therapy the effectiveness is judged by the clinic, laboratory data, the treatment dose is reduced to a prophylactic dose of 500 IU/day, which is taken for 2 years with the exception of the summer period. For rickets in premature infants, in addition to vitamin D, calcium glycerophosphate and calcium gluconate are used in a dose of 0.1 2 times a day for 3 weeks. To obtain the digestibility of calcium and phosphorus in the intestines and increase the reabsorption of phosphates in the kidneys - a citrate mixture:

Citric acid 2.1

Sodium citrate 3.5

Distilled water 100 ml.

1 teaspoon 3 times a day for 2 weeks. To normalize the function of the parathyroid glands and eliminate hypocalcemia, asparkam, panangin, 1% solution are prescribed magnesium sulfate, at a rate of 10 mg/kg for 3 weeks. In the phosphopenic variant with a severe course, it is necessary to improve energy metabolism: ATP 0.5 mg IM for 2 weeks. Potentiation static function: proserin 0.5 mg 3 times a day for 10 days. To stimulate metabolic processes - potassium orotate 10 mg/kg per day in 3 divided doses, cornitine hydrochloride 20% solution 10 drops 3 times a day for 3 months helps increase weight, reduce muscle hypotonia, normalization metabolic processes, 2 weeks after drug therapy- massage.

Prevention

Antenatal - a set of measures - sufficient time for a woman to stay in the fresh air for 1-4 hours. Her balanced diet, more regularly daily throughout pregnancy, multivitamins 1 tablet 1-2 times a day undevit.

Postnatal: proper nutrition of the child, timely introduction of supplements and complementary foods, sufficient exposure to fresh air, massage. To provide the woman with milk, the mother drinks multivitamins throughout the feeding period.

Specific prevention: vitamin D 500 IU/day for full-term babies from 3 weeks in the autumn-winter-spring period, not carried out from July to September (prevention for 2 years), if the child is bottle-fed, then a preventive dose taking into account vitamin D from the mixture, if it is not possible to calculate this, then the prophylactic dose is 250 IU/day. In premature infants, vitamin D from 7-10 days of age is 500 units/day for 2 years, regardless of the season, from 7 days to 4 months, vitamin E 5 mg/kg + calcium and phosphorus preparations. Children with anticonvulsant therapy 2000 units/day. Children with a decrease in the large fontanel or its early closure from 3-4 months. All children after severe rickets must be registered at a dispensary for three years; vaccinations are not contraindicated 1.5-2 months after treatment.

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Rickets (from the Greek word rhahis- spinal ridge), apparently, was already well known to doctors of ancient times. In the works of Soranus of Ephesus (98-138) and Galen (131-211), according to medical historians, there are descriptions of this disease. Soranus, whom I.V. Troitsky calls the first pediatrician of the “eternal city,” observed children in Rome with deformities of the legs and spine and attributed them to the early onset of walking. Galen, in his works on anatomy, described rachitic changes in bones.

It is possible that some skeletal changes caused by rickets were then taken for quite normal features child's body. In the paintings of old Danish, Dutch and German artists of the 15th-16th centuries. You can see children with obvious features of rickets - an Olympic forehead, deformation of the chest, thickened epiphyses of the limbs. In some contradiction with this is the assumption of E. M. Lepsky that before the 17th century. rickets was not a common disease, since there is no reliable data about it in the medical literature of those centuries; rather, we can assume that rickets was not mistaken for a disease. True, E.M. Lepsky points out that when examining bones belonging to different periods- from more ancient ones to the 16th century, obtained during archaeological excavations, it was extremely rare to find traces of rickets.

Beginning with the 17th century, people began to become particularly interested in rickets, and the interest of doctors and experimenters in it periodically manifests itself to a greater or lesser extent to this day.

A huge amount of literature is devoted to rickets. Many of the published works currently have, of course, only historical interest, but many have not lost their scientific and practical value even now. Rachitic deformations of the skeleton were described in detail and well in 1609 by the French physician Guilmot; Some other works of foreign doctors also date back to the first half of the 17th century: the clinical picture of rickets was described by Weistler and Butis. In 1650, the English anatomist and orthopedist Glisson, in his work, exhaustively described the clinical picture and pathological anatomy of rickets. Many valuable works were published in the 19th century, especially in the second half of it; These works supplemented and clarified the clinical picture of rickets, but did not introduce fundamentally new data that changed the results of Glisson’s classic studies.

In 1830, the work of G. Tikhomirov, “Rules on the method of healing the English disease,” appeared, and in 1843, the work of Elsasser, who focused on changes in the bones of the skull and described the softening of flat bones characteristic of rickets, which he called craniotabes.

Large and valuable works include the work of Kassovitz, who pointed out the seasonal nature of the appearance and exacerbation of rickets. This instruction at that time shed light on the etiology of rickets, and currently determines the doctor’s tactics in his preventive work. Kuttner wrote about this somewhat earlier, whose work attracted less attention from his contemporaries. He provided data on the number of children admitted to his supervision for 20 years with symptoms of rickets, for individual months of the year:

Pommer in 1885 clarified the picture of histological changes in bones during rickets.

These brief and, of course, far from complete historical information indicate the interest of foreign clinicians and anatomists in the study of rickets.

Of our domestic authors, S. F. Khotovitsky was the first in 1847 to describe in detail in his manual “Pediatrics” the clinical picture of rickets and some aspects of the etiology and pathogenesis of the disease. A little earlier in the article "English Disease", placed in " Encyclopedic Dictionary Plushara", S. F. Khotovitsky expresses absolutely correct and for that time very progressive thoughts about rickets. This work well outlines the clinical picture, preventive measures and treatment of rickets; S. F. Khotovitsky emphasizes that when treating rickets, the main attention should be paid to medications, but hygienic measures and nutrition.When describing the clinical picture, he points not only to changes in the skeleton, but also to big belly, hydrocephalus, the fact that with rickets “profuse sweat of a special smell often appears, especially on the forehead,” and due to deformations of the chest “short, unfree breathing occurs,” etc. He points to the harm of starchy diet, overfeeding, untidiness , dampness, lack of movement and sunlight and many others negative points, which we are talking about now.

Since then, rickets has continued to attract the attention of Russian researchers, who with their work contributed a lot of valuable information to the understanding of the essence and clinical picture of the disease. N. S. Korsakov showed in his dissertation that a lack of lime cannot be considered the main cause of rickets.

A. A. Kisel in his doctoral dissertation “On the issue of pathoanatomical changes in the bones of growing animals under the influence minimum doses phosphorus" from 1887 refuted the conclusions of Wegner, who injected experimental animals with yellow phosphorus and believed that large doses cause changes in them resembling rachitic ones, and small doses give reverse effect- sclerosis of bones. Given these data, Kassovitz suggested treating children with rickets with phosphorus. A. A. Kisel, based on his research, denied its therapeutic value in the treatment of the disease; this was an original and bold statement, if we remember that then the main method of treating rickets, recognized by everyone, was the administration of phosphorus in fish oil.

V.P. Zhukovsky wrote in his dissertation about the spread of rickets among children and about the conditions favorable to this.

Along with clinicians, many domestic representatives were interested in rickets issues theoretical disciplines. It is necessary to mention the research of L.L. Levshin, who proved the fallacy of the views of many experimenters who mistook the phenomena of osteoporosis that arose in animals that received food poor in lime for rickets. He showed that in rickets there is a significant deposition of osteoid tissue, which distinguishes rickets from any other osteoporotic bone. R. Streltsov's research on histological changes in bones during rickets is original. He refuted the view of Virchow, who considered the inflammatory process in the bone marrow to be the main factor in the pathogenesis of rickets. R. Streltsov was one of the first to prove that thickening of the epiphyseal cartilage is the result of delayed bone formation during rickets.

It should be noted that V.V. Pashutin, the largest Russian pathophysiologist, attached great importance domestication in the pathogenesis of rickets; he believed that changes in the bones of the experimental animals with which Wegner worked were largely due to keeping them indoors.

The studies of I. A. Shabad on the peculiarities of phosphorus-calcium metabolism, and Gurji - on the peculiarities of alkaline-acid balance in children suffering from rickets, brought us much closer to understanding the pathogenesis of rickets. These works have not lost their significance to this day.

I. A. Shabad was the first to show that the positive balance of phosphorus and lime, which is observed in healthy children, can become negative in children with rickets; he also found that it was positive therapeutic effect the administration of phosphorus in fish oil to children with rickets depends not on the phosphorus, but on the fish oil with which it is given. By this he confirmed the experimental data of A. A. Kisel, mentioned above.

M. S. Maslov in his dissertation “On biological significance phosphorus for a growing organism", written in 1913, noted the enormous importance of phosphates for a growing organism, the connection of their exchange with intracellular enzyme systems and the harm to a growing organism of prolonged monotony milk feeding, causing depletion of the body in phosphorus and a decrease in the activity of intracellular enzymes.

Numerous studies by radiologists have significantly enriched our knowledge about the dynamics bone changes in children suffering from rickets; X-rays, especially repeated ones, are of great importance for the diagnosis, assessment of the activity of the process and the effectiveness of the therapy.

The social significance of rickets was clear to domestic pediatricians. At the V Pirogov Congress, N. I. Bystrov reported on rickets among peasant children; At the VI and IX Pirogov congresses, A. A. Kisel spoke about rickets as a social disease.

Start new era in the study and understanding of the etiology and pathogenesis of rickets dates back to 1919. In this year, Huldshinsky showed that rickets in children is cured under the influence of the rays of an artificial mountain sun (quartz lamp), and Mellanby, in an experiment on dogs, proved that severe rickets caused in them a special rachitogenic diet, cured with fish oil.

Iversen and Lenstrup in 1919 established the presence of hypophosphatemia in rickets. McCollum and his colleagues in 1921, using a special diet, managed to induce rickets in young rats; the use of these animals greatly facilitated the study of experimental rickets. Hess found that not all ultraviolet rays have antirachitic activity, but only those with a length of 280-310 mm. In 1924, Hess and Stenbock showed that under the influence of irradiation with ultraviolet rays, some types of food acquire a new property for them - antirachitic activity; a little later, Hess was able to find out that this was due to the presence of lipoids, especially cholesterol, in them. Further research by Hess clarified that ergosterol, contained in small amounts in cholesterol, acquires antirachitic properties.

Mellanby already suspected that the positive effect of fish oil in the treatment of rickets was explained by the presence of some vitamin in it, and in 1922 McCollum and his colleagues proved that this effect does not depend on the influence of the antixerophthalmic factor contained in it, which is destroyed when air is passed through heated fish oil, and from another vitamin specific to rickets, which has a therapeutic effect in the treatment of children with rickets, as well as experimental rickets in animals. This vitamin was named vitamin D. Only in 1936 did Windows establish structural formula vitamin D2 and D3.

All these studies made it possible to put the prevention and treatment of rickets in children on a completely new and theoretically grounded basis.

Since that time, research into experimental rickets in animals has become especially widespread.

In connection with these successes, a large number of works by domestic and foreign authors devoted to rickets appeared. It is necessary to mention monographs and individual articles by domestic authors - A. N. Antonov, S. O. Dulitsky, E. D. Zabludovskaya, P. V. Kuskov, E. M. Lepsky, M. S. Maslov, P. S. Medovikov , K. A. Svyatkina, I. Ya. Serebrisky, G. N. Speransky, A. F. Tour, A. M. Khvul, I. V. Tsimbler, S. Ya. Shafershtein and many others.

The large monographic works of M. N. Bessonova, E. M. Lepsky and their collaborators that have appeared recently have already been mentioned above. Despite such fruitful centuries-long work of scientists and doctors, clinicians and theoreticians - experimenters around the world on the problem of rickets, many issues of the clinic, etiology, pathogenesis, prevention and treatment of rickets still, as mentioned above, cannot be considered finally resolved.

Details

Diagnosis of the underlying disease:

Accompanying illnesses:

Patent foramen ovale

I. Passport part

Full name – ---.

Floor– male

Age – 10 years(20.11.2000)

Permanent residence- Moscow

Educational institution - school, 5th grade

receipt date – 08.09.2011

Date of supervision – 20.09.2011

II. Complaints

For nagging, intermittent pain of moderate intensity in the epigastric region, umbilical region, in the right hypochondrium, occurring soon after eating and self-limiting after 1-2 hours, accompanied by nausea and vomiting.

III. History of present illness

(Anamnesis morbi)

Since the age of 5 he has suffered from abdominal pain, often due to poor diet. 09/08/2011 I felt nausea, accompanied by abdominal pain and periodic belching. In connection with the above complaints, on September 20, 2011, he was urgently hospitalized in the children's department of the Central Clinical Hospital.

IV. Life story

(Anamnesis vitae)

Antenatal period. Mother's second pregnancy. The course of pregnancy is physiological. Working and living conditions during pregnancy are satisfactory, nutrition during pregnancy is good. The birth was normal, planned caesarean section, without complications.

Characteristics of the newborn. He was born full-term, birth weight 3300 g, length at birth 53 cm.

Apgar score 9/10. He immediately screamed, the scream was loud.
Baby feeding: breastfeeding up to 6 months.
Information about the dynamics of physical and psychomotor development. Birth weight - 3300. He has been holding his head since 2 months. Sitting since 6 months. He has been walking since he was 11 months old. Teeth - from 7 months. By one year - 8 teeth. First words - from 1 year. Behavior in the family and in the team is appropriate for his age, he has been attending school since he was 6 years old. His school performance is satisfactory, he is in 5th grade, grade “4”.

Epidemiological anamnesis.

Chicken pox, tonsillitis at 7 years old, ARVI rarely gets sick. In contact with febrile and infectious patients, in endemic and epizootic foci during the last three months was not.

Past illnesses.

Observed by a gastroenterologist and cardiologist. Allergic reactions on food products, medications and denies other means.

Preventive vaccinations. In the first 12 hours of life - the first vaccination against viral hepatitis B;
3-7 days of life: vaccination against tuberculosis;
1 month: second vaccination against viral hepatitis B;
3 months: first vaccination against diphtheria, whooping cough, tetanus, polio;
4.5 months: second vaccination against diphtheria, whooping cough, tetanus, polio;
6 months: third vaccination against diphtheria, whooping cough, tetanus, polio; third vaccination against viral hepatitis B;
12 months: vaccination against measles, rubella, mumps;
18 months: first revaccination against diphtheria, whooping cough, tetanus, polio;
20 months: second booster vaccination against polio;
6 years: revaccination against measles, rubella, mumps;
7 years:; second revaccination against diphtheria, tetanus.

Mantu's latest reaction, according to his parents, is negative.

V. Present state (Status praesens)

General inspection

Height 144 cm. Above average height
Weight 39 kg. Weight corresponds to average age indicators

Development is harmonious, above average.

The condition is satisfactory. Consciousness is clear. The reaction to the environment is adequate. Position active.

Body weight – 39 kg. Physical development above average. The physique is normosthenic. Body temperature 36.6 O C.

The skin is pale pink, on the left side of the chest - birthmark 5 cm in diameter, coffee-with-milk color, skin intact. Subcutaneous tissue underdeveloped. Visible mucous membranes without acute catarrhal changes. Subicteric sclera.

Lymphatic system.

Lymph nodes are single, elastic in consistency, painless, mobile.

Skeletal system: normal posture. The morphophenotype is athletic.

Respiratory system

Breathing through the nose is free, there is no discharge. The voice is clear and clear. The chest is normosthenic, regular in shape. The supraclavicular and subclavian fossae are sunken. The costal arches are straight, the intercostal spaces are not enlarged. The epigastric angle is straight. The shoulder blades and collarbones do not protrude. The chest is symmetrical. Chest circumference 56cm. breathing excursion 5 cm. Mixed breathing type. Respiratory movements are symmetrical, auxiliary muscles are not involved. The number of respirations is 18 per minute at rest. Breathing is rhythmic, shallow, with equal duration of the inhalation and exhalation phases. The chest is painless on palpation. Voice tremors on symmetrical areas of the chest the same, not changed. A clear pulmonary percussion sound is detected over the entire surface of the chest.

Upper border of the lungs:
front height of tops	2.5 cm above the collarbone	2.5 cm above the collarbone
back height of tops		at the level of the spinous process of the VII cervical vertebra
Lower border of the lungs:
along the parasternal line	VI intercostal space	not defined
along the midclavicular line		not defined
along the anterior axillary line
along the midaxillary line
along the posterior axillary line
along the scapular line
along the paravertebral line	spinous process XI thoracic vertebra	spinous process XI thoracic vertebra

Vesicular breathing is heard over the entire surface of the chest. No wheezing. Bronchophony in symmetrical areas of the chest is the same and not changed.

The cardiovascular system

The veins of the neck do not swell. There is no cardiac hump, the apical impulse, cardiac impulse and epigastric pulsation, pulsation in the 2nd intercostal space on the right, left, and in the jugular fossa are not visually detected. Atypical pulsation: no paradoxical, negative pulsation. The apical impulse is palpated in the 5th intercostal space along the midclavicular line, not strengthened, localized. Area less than 1 cm2. Trembling in the area of ​​the heart at the apex, at the base of the heart is not detected. Pathological pulsation in the second intercostal space on the right, left, in the jugular fossa is not detected. There is no palpation tenderness in the precordial area.

Borders relative stupidity hearts.

The boundaries of relative dullness of the heart are not expanded upon percussion.

The rhythm is correct, the number of heartbeats is 86 per minute. At all points of auscultation I and II, the sounds are sonorous, rhythmic, there is no splitting or bifurcation. No additional tones are heard. A short soft systolic murmur is heard at the apex. Arterial pulse on radial arteries the same on the right and left, rhythmic, satisfactory filling and tension, 86/min. There is no pulse deficit. Blood pressure on the brachial arteries is 112/62 mm Hg.

Digestive system

Appetite is good, no nausea or vomiting. Stool 1 time per day, moderate amount, formed, brown. On examination: the tongue is moist, with a delicate white-yellow coating. Milk teeth. Gums, soft, solid sky pale pink, clean. There is no bad breath. The abdomen is not swollen, of regular shape, symmetrical, and actively participates in the act of breathing. There are no hernias of the white line and umbilical ring on the anterior abdominal wall. The navel is retracted. A tympanic percussion sound is detected over the entire surface of the abdomen; free liquid V abdominal cavity not determined. On superficial palpation, the abdomen is soft, discrepancies of the rectus abdominis muscles, hernias of the white line, umbilical hernia not determined. Shchetkin-Blumberg's symptom is negative. There is pain in the epigastric and periumbilical region. Methodical deep sliding palpation according to Obraztsov-Strazhesko is difficult due to pain in the epigastric and periumbilical region. Peristalsis is heard over the entire surface of the abdomen, 1-2 peristaltic sounds per 1 minute.

Liver and gallbladder

There is a bulge in the right hypochondrium; there is no restriction in breathing in this area. Dimensions of the liver according to Kurlov: along the right midclavicular line - 7 cm, along the anterior midline - 6 cm, along the left costal arch - 5 cm. The edge of the liver during inspiration: +1 cm from under the costal arch. The gallbladder is not palpable, there is no pain. Kehr's, Ortner's, and phrenicus symptoms are negative.

Spleen

There is a bulge in the left hypochondrium; there is no restriction in breathing in this area. Upon percussion, the longitudinal size of the spleen along the X rib is 7 cm, the transverse size of the spleen is 3 cm. The spleen is not palpable.

Pancreas

There is no pain in the area of ​​projection onto the anterior abdominal wall, no enlargement or hardening of the pancreas.

urinary system

Urination is free and painless. There are no dysuric disorders. There is no swelling, bulging, hyperemia of the skin, or limited protrusions in the suprapubic area. The lumbar region is painless when tapped on the right and left. The kidneys are not palpable in a standing or lying position. The bladder is not palpable. Pain on palpation at the costovertebral point and along the ureter is not determined

Neuropsychic state and sensory organs

Consciousness is clear, behavior is adequate. The patient is calm and sociable. Attention and memory, intelligence correspond to the age norm. There are no speech impairments. Sleep is normal. Violations motor functions No. Mixed dermatographism, no sweating. Taste, smell, and hearing are not impaired. Sensitivity is preserved. Tendon reflexes are alive. Severe neurological symptoms, meningeal symptoms No.

Endocrine system

There are no disturbances in growth, physique and proportionality of individual parts of the body. Thirst, hunger, constant feeling There is no fever, chills, cramps, or increase in body temperature. The thyroid gland is not enlarged

Survey plan

1. RW, markers of hepatitis B and C

2. General blood test

3. Biochemical analysis blood

4. General urine test

5. Coprogram, feces for worm eggs and protozoa + occult blood

6. Scraping for enterobiasis

7. Ultrasound of the abdominal cavity

8. Endoscopy (indications to be discussed during observation, examination dynamics) + biopsy

9. Consultations with doctors of exercise therapy, physical therapy, gastroenterologist, nutritionist.

10.Urine analysis for uroamylase

Laboratory data, instrumental methods research and specialist consultations

1) General blood test

2) Biochemical blood test

3) General urine test

4) Stool examination

5) Examination of scrapings for enterobiasis

No pinworm eggs found (N).

6) Ultrasound of the abdominal cavity and retroperitoneal space

Liver: the size of the lobes is not changed. Anteroposterior size right lobe 8.9 cm, anteroposterior size of the left lobe 5.1 cm. The contours of the liver are smooth, clear, the angles are sharp, the line of the diaphragm is clear. The structure of the parenchyma is homogeneous, without signs focal changes. Echogenicity is normal. The diameter of the main trunk of the portal vein is 0.9 cm (N up to 1.25 cm). Progress of the main vascular structures the liver is not impaired. The vascular pattern of the liver parenchyma is normal. The intrahepatic bile ducts are not dilated. No additional organized inclusions are detected in the projections of the liver.

The gallbladder, with two bends in the body and in the neck, looks hypotonic, measuring 5.1x1.93 cm. The wall is not thickened or compacted. No intraluminal or parietal formations were identified.

Common bile duct with a diameter of up to 0.3 cm, not dilated. No intraluminal echostructures were identified.

Pancreas: regular form, segment sizes: head 19 mm, body 11 mm, tail 19 mm. The contours are smooth, clear, and preserved. The parenchyma is homogeneous, without signs of focal changes. The echogenicity is similar to that of the liver.

Spleen: the topography is not changed, the contours are smooth and clear. Dimensions: 94x35mm. The pattern of structures is well differentiated. The parenchyma is homogeneous, without focal changes and additional inclusions.

No free fluid was detected in the abdominal cavity.

Kidneys: the topography is not changed, the contours are smooth, clear, dimensions: right 8.9x4.6 cm, left 8.7x3.8 cm. The parenchyma of both kidneys is structurally unchanged. The collecting system on both sides is not expanded. Cortico-medullary differentiation is clearly visible. With ultrasound angiography, blood flow on both sides is unchanged and can be traced to the cortical layers. The bladder is not full.

Conclusion: deformation of the gallbladder.

The esophagus is freely passable, its mucous membrane is not changed, the cardia closes. In the antrum of the stomach there are large hemorrhagic erosions with hematin. The pylorus is passable, the bulb and descending section of the 12th colon are without features.

Conclusion: erosive hemorrhagic antral gastritis.

8) Biopsy examination

Object: from the mucous membrane of the antrum of the stomach + on HP

Type of biopsy: diagnostic

Number of studies (fragments): 2

Clinical diagnosis: hemorrhagic gastritis antrum of the stomach

Microdescription: separate strips of desquamated integumentary epithelium and mucus. No CB was detected on the surface

CLINICAL DIAGNOSIS AND ITS RATIONALE:

Diagnosis of the underlying disease:

Chronic erosive-hemorrhagic antral gastritis, acute phase.

Concomitant diseases: Patent foramen ovale

Rationale for diagnosis:

The diagnosis of chronic erosive-hemorrhagic antral gastritis, acute phase, was made on the basis of:

Complaints about:

Upon admission: nagging, intermittent pain of moderate intensity in the epigastric, periumbilical region, in the right hypochondrium, arising soon after eating and self-limiting after 1-2 hours, accompanied by nausea and vomiting

At the time of inspection he had no active complaints.

History of present illness:

Since the age of 5 he has suffered from abdominal pain, often due to poor diet.

Clinical examination data:

Pain in the epigastric and periumbilical region on superficial palpation;

Instrumental examination data:

Conclusion of endoscopy (Chronic erosive-hemorrhagic antral gastritis)

Biopsy examination (hemorrhagic gastritis of the antrum of the stomach)

TREATMENT

1) Diet No. 5

2) Omez 20 mg 2 times a day (morning and evening)

3) Maalox 15 ml 3 times a day before meals

4) No-spa 1 tablet 3 times a day

5) Motilium 1 tablet 3 times a day after meals

Observation diaries

Temperature: 36.8 degrees C

The condition is satisfactory. No complaints. The skin, pharynx and visible mucous membranes are clean.

Appetite preserved.

Very often on the playground, in the square or in the park you can hear young mothers discussing rickets. Some believe that there is nothing wrong with it, that this diagnosis is made to many children and does not require any treatment. Others are very worried and follow all the doctor’s orders, use traditional methods, grandmothers' recipes.

medical history
So what is rickets? Rickets is impaired mineralization of growing bone, leading to disturbances in skeletal formation in early childhood. In other words, this is a disease caused by a temporary discrepancy between the needs of a growing organism for calcium and phosphorus and the insufficiency of the systems that ensure their delivery to the child’s body.
Rickets is a disease known since ancient times. In the 2nd century BC, Soranus of Ephesus and Galen described rachitic changes in the skeletal system. Around the 15th-16th centuries, rickets was a fairly common disease among young children, especially from large (at that time) cities in Europe. It is no coincidence that many famous Dutch, Flemish, German and Danish artists of that time often depicted children with typical signs of rickets (overhanging brow ridges, flattened back of the head, flattened belly, twisted limbs). A classic example is the painting “Madonna and Child” (1512) by the immortal Albrecht Durer. And even now rickets is a fairly common disease. It affects from 20 to 60% of Russian children.

importance of vitamin D
As is known, vitamin D enters the human body through food, both plant and vegetable ( vegetable oil, wheat germ, nuts) and animal (dairy products, fish oil, butter, egg yolk) origin, and is also produced in the skin under the influence ultraviolet rays. Most meaningful forms vitamin D are ergocalciferol (vitamin D2) and cholecalciferol (vitamin D3). However, research by scientists has found that these vitamins have very little biological activity in the human body. The main effect on organs is exerted by their metabolic products, which are formed in the liver and kidneys as a result of certain biological transformations. They determine the main function of vitamin D in the body - maintaining phosphorus-calcium metabolism at the required level. When calcium and phosphorus in the blood decrease as a result of insufficient intake from food or impaired absorption in the intestines, minerals are “washed out” from the bones.

Causes of calcium and phosphorus deficiency
Prematurity, the birth of children from multiple pregnancies and babies with large body weight can contribute to the occurrence of deficiency of phosphorus and calcium compounds. Insufficient intake of minerals from food (early feeding with unadapted products such as whole cow's milk), late introduction of complementary foods (after 6 months), introduction of carbohydrate-rich foods (semolina porridge) in the form of complementary foods, adherence to strict vegetarianism (complete exclusion of meat products from the diet), violation absorption of calcium and phosphorus in the intestine due to organ disease gastrointestinal tract or enzyme immaturity can also lead to rickets. In addition, there may be individual characteristics of the child, such as dark skin color (this reduces the production of vitamin D in the skin), hereditary characteristics vitamin D metabolism, congenital disorders functions of the intestines, liver and kidneys, predisposing to disturbances in the metabolism of calcium, phosphorus and vitamin D in the baby’s body.

first signs of rickets
The first signs of rickets can appear as early as the 2-3rd month of a baby’s life, and even earlier in premature babies. Often the first symptoms of the disease (the so-called initial period of rickets), which parents notice, are sleep disturbances (sleep becomes restless, anxious, with startlings), irritability, tearfulness, frequent startling of the child even with a low sound. The baby develops increased sweating, especially during sleep or feeding. The face and body sweat the most hairy part heads. Due to shifts in metabolic processes in the body, sweat becomes “sour”, irritates the skin, and the child begins to rub his head on the pillow, which causes baldness at the back of the head. Urine may also have sour smell and irritates the baby's skin, often causing diaper rash. When examining the baby, the doctor, as a rule, notes a slight softening of the skull bones that form the edges of the large fontanel and sutures. If treatment is not started at this stage and the causes contributing to the development of rickets are not eliminated, then clinical manifestations the diseases begin to gradually increase, and the child develops pronounced bone changes.

the height of the disease and the disappearance of symptoms
The peak period of the disease most often occurs at the end of the first half of the baby’s life. The softness and pliability of the edges of the large fontanelle is accompanied by softening of the bones of the skull: flattening of the back of the head appears, and asymmetry of the head occurs. As a result of excessive growth of non-calcified bone tissue(the growth of which normally stops after calcification), the child’s frontal and parietal tubercles begin to protrude, and the skull takes on a peculiar shape. In addition, seals appear on the ribs in the form of “rachitic rosaries”, and on the wrists - “rachitic bracelets”.
In the second half of life, when the load on the bones increases, curvatures of the spine (“rachitic hump”), the chest (it can be pressed inward or protrudes), and the pelvis (narrow) appear. irregular shape pelvis (“flat-rachitic pelvis”). As children begin to walk independently, their legs often become bent, taking on an O-shape and, less commonly, an X-shape, and flat feet develop. As a result of muscle weakness, a large belly (“frog” belly) appears, increased mobility in the joints, the child begins to lag behind in the development of motor skills (late starts to roll over on his stomach and back, sit, crawl, stand, walk). In addition, in children with manifestations of rickets, teething is delayed, and the functioning of internal organs often occurs: lungs, heart, gastrointestinal tract (tendency to constipation).
However, the symptoms of the disease gradually subside and a period of recovery begins. At the same time, the child’s well-being improves, changes in the nervous system and internal organs disappear, the child begins to sit, stand, and walk better, although muscle tone disorders and bone deformations persist for a long time, some throughout life. The period of residual effects is characterized by the fact that signs of active rickets are no longer present, but bone deformations remain: big head, deformed chest, narrow pelvis, flat feet, malocclusion.

treatment of the disease
Treatment of children with manifestations of rickets should be comprehensive, taking into account the reasons that led to the development of the disease. It must be started when the first symptoms of the disease appear and carried out for a long time, achieving complete cure child. Therapy is prescribed by a pediatrician. It is customary to distinguish specific and nonspecific methods of treating rickets. Non-specific methods include a properly organized daily routine with sufficient exposure of the child to the fresh air; nutrition aimed at normalizing disrupted metabolic processes in the baby’s body; regular exercise, massage, swimming.
Specific treatment of rickets involves the prescription of vitamin D preparations, the choice of which depends on the severity of the disease, the nature of the damage to internal organs and the age of the children. It is recommended to use 2000 to 5000 IU of vitamin D per day for 30-45 days. Then the dose is reduced to prophylactic (500 IU daily) and the drug is used for two years and in the 3rd year of life in winter.
Vigantol (Cholecalciferol) is an oily solution for oral administration containing about 650 IU in 1 drop active substance. The drug can be used both for the prevention and treatment of rickets. Vigantol is oil solution, it is well absorbed due to its special fat composition. This circumstance allows it to be used as a drug for the treatment of phosphorus-calcium metabolism disorders in patients with impaired digestion and absorption syndrome.
A differentiated choice of vitamin D preparations involves the use of D3 (aqueous) solution of cholecalciferol in children with diseases of the gastrointestinal tract and liver, kidney diseases and urinary tract. Along with vitamin D, children are prescribed calcium supplements.

Prevention of rickets
To ensure that the child does not have problems after birth, during pregnancy a woman should monitor her diet and health (preventing the birth of a premature baby), and adhere to the correct daily routine. Recommended for a newborn natural feeding, timely introduction of complementary foods is necessary, the baby needs walks, massage, and gymnastics. A nursing mother should also take care of her diet; she should remember that everything necessary substances The baby receives it through breast milk. The doctor also prescribes vitamin D preparations in prophylactic doses.