Infant Rahit is widespread in children of the first years of life. The first mention of Rakhit is found in the writings of Senna Efesse (98-138 AD), which revealed deformation lower extremities And the spine in children. Galen (131-201 AD) gave a description of the richite changes of the bone system, including the deformation of the chest. In the Middle Ages, Rakhit called English disease, since it was in England that it was the prevalence of its heavy forms, which was associated with insolation in this climatic zone. A complete clinical and pathologist of Rakhita made the English orthopedist Francis Glisson in 1650 in his opinion, the main risk factors for rickets in children are burdened heredity and improper nutrition of the mother. In 1847, in the book "Pediyatrika" S.F. Hotovitsky described not only the defeat of the bone system during rickets, but also changes in the gastrointestinal tract, vegetative disorders, muscle hypotension. In 1891 N.F. Filatov noted that Rakhit is a common disease of the body, although manifests, mainly a kind of bone change.
According to modern ideas, Rahit is a disease characterized by a temporary inconsistency between the needs of the growing organism in phosphorus and calcium and the insufficiency of the systems of their transportation in the body. This disease of the growing organism, due to disruption of methasophilic methasis, the main clinical syndrome of which is the defeat of the bone system (violation of the formation, proper growth and mineralization of bones), in which the pathological process is localized mainly in the field of metaepyyphysis. bones. Since the growth and speed of restructuring the bones are highest in early childhood, the bone lesions are most pronounced in children 2-3 years. Rahit is a polyfactory metablastic disease, in the diagnosis, prevention and treatment of which all the factors of pathogenesis should be taken into account: Insufficiency and imbalance of calcium and phosphorus with food, the immaturity of the endocrine system of the child, concomitant diseases, etc. In addition to the pathology of phosphorous calcium metabolism, protein exchange violations and trace elements (magnesium, copper, iron, etc.), multivitamin failure, activation of lipid peroxidation.
Code of the ICD-10
E55.0. Rahit active.
EPIDEMIOLOGY
Rahit is found in all countries, but especially often among the northern peoples who live in conditions of lack of sunlight. Children, born in the fall and winter, are getting rickets more often and harder. At the beginning of the XX century. Rakhit noted in 50-80% of children early age In Western Europe. Up to 70% of children in Russia these years also had Rahit. According to A.I. Ruffle (1985), Rickets in children of the first year of life meets up to 56.5%, according to S.V. Maltseva (1987), its prevalence reaches 80%. The most difficult disease occurs in premature babies.
To date, classic (vitamin D-deficient) Rahit occupies a significant place in the structure of the morbidity of young children. In Russia, its frequency in last years ranges from 54 to 66%. According to pediatricians of Moscow, the classic Rahit is currently found in 30% of young children. This indicator can be considered understated, since only heavy and medium-sized forms of the disease are recorded. In developed countries, which introduced the specific prophylaxis of rickets with vitamin D and the vitaminization of baby food products, heavy forms of rickets have become a rarity, but subclinical and radiological manifestations remain widespread. So, in France, the hidden deficiency of vitamin D was revealed in 39%, and explicit clinical manifestations - in 3% of children who came to hospitals about various diseases. In the northern provinces of Canada, hypovitaminosis D was found in 43% of children surveys. IN southern countriesDespite the sufficient intensity of ultraviolet irradiation, Rakhit remains a very common disease. In Turkey, Rahit was detected in 24% of children aged 3-6 months, although the introduction of prevention by vitamin D made it possible to reduce its prevalence up to 4%.
Rakhit (from Greech. Rhachis - "Range", "Spine") was known to doctors in ancient times. In 1650, English Anata and Orthopedist Glisson described the clinical picture of Rakhit, called the "English disease", "slum disease". Significant contribution to the study of Rakhita was made by domestic scientists - Pediatricians: N.F. Filatov, A.A. Kisel, G.N. Speransky, A.F. Tour, K.A. Svakkin, E.M. Lukyanova.
Violation of costh formation is localized mainly in the area of \u200b\u200bepimetafiz bones (growth zone). Since the growth of bones and the speed of their restructuring (remodeling) are highest in early childhood, the bone manifestations of Rakhit are most pronounced in children of the first 2-3 years of life. For rickets, there are also changes in other organs and systems, a decrease in the immune reactivity of the child.
Infant Rahit is widespread in children of the first years of life. The first mention of Rahit is found in the works of Senna Efesse (98-138 AD), which revealed the deformation of the lower extremities and the spine in children. Galen (131-201 AD) gave a description of the richite changes of the bone system, including the deformation of the chest. In the Middle Ages, Rakhit called English disease, since it was in England that it was the prevalence of its heavy forms, which was associated with insolation in this climatic zone. Full clinical and pathoanomatic description of Rakhita made the English orthopedist Francis Eppisson in 1650 in his opinion, the main risk factors for rickets in children are burdened heredity and improper nutrition of the mother. In 1847, in the book "Pediyatrika" S.F. Hotovitsky described not only the defeat of the bone system during rickets, but also changes in the gastrointestinal tract, vegetative disorders, muscle hypotension. In 1891 N.F. Filatov noted that Rakhit is a common disease of the body, although manifests, mainly a kind of bone change.
According to modern ideas, Rahit is a disease characterized by a temporary inconsistency between the needs of the growing organism in phosphorus and calcium and the insufficiency of the systems of their transportation in the body. This disease of the growing organism, due to disruption of methasophilic methasis, the main clinical syndrome of which is the defeat of the bone system (violation of the formation, proper growth and mineralization of bones), in which the pathological process is localized mainly in the field of metaepyyphysis. bones. Since the growth and speed of restructuring the bones are highest in early childhood, the bone lesions are most pronounced in children 2-3 years. Rahit is a polyfactory metablastic disease, in the diagnosis, prevention and treatment of which all the factors of pathogenesis should be taken into account: Insufficiency and imbalance of calcium and phosphorus with food, the immaturity of the endocrine system of the child, concomitant diseases, etc. In addition to the pathology of phosphorous calcium metabolism, protein exchange violations and trace elements (magnesium, copper, iron, etc.), multivitamin failure, activation of lipid peroxidation.
Code of the ICD-10
E55.0. Rahit active.
Epidemiology Rakhita
Rahit is found in all countries, but especially often among the northern peoples who live in conditions of lack of sunlight. Children, born in the fall and winter, are getting rickets more often and harder. At the beginning of the XX century. Rakhit was noted in 50-80% of young children in Western Europe. Up to 70% of children in Ukraine these years also had Rahit. According to A.I. Ruffle (1985), Rakhit in children of the first year of life occurs to 56.5%, according to St. Maltseva (1987), its prevalence reaches 80%. The most difficult disease occurs in premature babies.
To date, classic (vitamin D-deficient) Rahit occupies a significant place in the structure of the morbidity of young children. In Russia, its frequency in recent years ranges from 54 to 66%. According to pediatricians of Moscow, the classic Rahit is currently found in 30% of young children. This indicator can be considered understated, since only heavy and medium-sized forms of the disease are recorded. In developed countries, which introduced the specific prophylaxis of rickets with vitamin D and the vitaminization of baby food products, heavy forms of rickets have become a rarity, but subclinical and radiological manifestations remain widespread. So. In France, the hidden deficiency of vitamin D was detected in 39%, and explicit clinical manifestations - in 3% of children who came to hospitals about various diseases. In the northern provinces of Canada, hypovitaminosis D was found in 43% of children surveys. In southern countries, despite the sufficient intensity of ultraviolet irradiation, Rahit remains a very common disease. In Turkey, Rahit was detected in 24% of children aged 3-6 months, although the introduction of prevention by vitamin D made it possible to reduce its prevalence up to 4%.
Rahit, especially the average and severe degree, transferred in early childhood, can have an adverse effect on the subsequent development of children. Such children develop a disorder of posture, flatfoot, flattening and deformation of pelvic bones, caries, myopia. The role of rickets in the development of osteopyings and osteoporosis, which are widespread in adolescents are proved. The consequences of vitamin D deficiency in childhood are given in Table. 11-1.
Consequences of vitamin D deficiency
Causes of Rakhita
The main etiological factor of Rakhita is a deficiency of vitamin D. At the same time, Rahit is considered as a multifactorial disease in which the inconsistency arises between the high need of a growing child in phosphorous calcium salts and the insufficient development of regulatory systems that ensure the flow of these salts in the tissue.
There are two ways to provide the body with vitamin D: admission to food and education in the skin under the influence of ultraviolet rays. The first way is associated with the flow of cholecalciferol (vitamin D3) with animal products (cod liver, fish caviar, egg yolk; in less degree - female and cow's milk, butter). IN vegetable oils Ergocalciferol (vitamin D2) can occur. The second path is associated with the formation of vitamin D in the skin of 7-dehydroholestertern under the influence of ultraviolet rays with a wavelength of 280-310 μm. Previously, they believed that these two ways to provide vitamin D are equal. However, recently it became known that more than 90% of vitamin D is synthesized during ultraviolet irradiation, and 10% - comes with food. Under favorable conditions in the skin of the child, the required amount of vitamin D is formed. With insolation due to insolation due to climatic features (Skylessness atmospheric air, cloudiness, fogs), the intensity of vitamin D synthesis decreases.
Education of active metabolites vitamin D
Entering the body, vitamin D is converted into more active metabolites by complex transformations in the liver and kidneys.
The first step of activation is associated with the fact that the vitamin D entering the digestive tract or the resulting vitamin D is transported to the liver, where, under the influence of the enzyme 25-hydroxylase, it turns into 25-hydroxycholecalciferol, or calcidiol, is the main form of vitamin D circulating in the blood. In healthy children, the content of 25-hydroxycholecalciferol in serum is about 20-40 ng / ml.
The second stage of the metabolism of vitamin D is re-hydroxylation in the kidneys, where the 25-hydroxycholecalciferol is transferred with a vitamin D-binding protein (transcalciferine). At the level of kidney mitochondria, the most active metabolite is formed - 1.25-dihydroxycholecalciferol, or calcitriol, as well as 24,25-dihydroxycholecalciferol. The formation of the main metabolite - calcitriol - occurs with the participation of the renal enzyme 1-A-hydroxylase. The concentration of calcitriol in the blood plasma is about 20-40 pg / ml.
The main physiological function of vitamin D
The main physiological function of vitamin D is the control of calcium ions in the body (hence the name "calciferol" - "carrying calcium") - is carried out by regulating the absorption of calcium ions in the intestine and rehabilitation in renal channels, as well as stimulating bone mineralization. With a decrease in the level of calcium and inorganic phosphates in the blood or when strengthening the secretion of the parathyroid hormone, the activity of the renal 1-a-hydroxylase and the synthesis of 1.25-dihydroxycholecalciferol is sharply rising.
With normal I. increased levels The calcium and phosphorus in the plasma is activated by another kidney enzyme - 24-hydroxylase, with the participation of which 24,25-dihydroxycholecalciferol is synthesized, which promotes calcium deposition and phosphates in bone tissue and the overwhelming secretion of the parathyroid hormone.
In recent years, the presentation of the role of vitamin D has been significantly supplemented with data on the transformation of this vitamin in the body, which led to a change in vitamin D views as a typical vitamin. According to modern ideas, vitamin D should be considered powerful hormonally active compoundSince, like hormones, it affects specific receptors. It is known that the metabolite of vitamin D (1,25-dihydroxycholecalciferol) transmits a signal to the gene device (DNA) cells and activates genes controlling the synthesis of functional transport proteins for calcium ions. The target organs for this metabolite - intestines, kidneys, bones. In the intestine, vitamin D stimulates the absorption of calcium and equivalent quantities of inorganic phosphates. In the kidneys, with its participation, there is an active reabsorption of calcium and inorganic phosphates. Vitamin D regulates mineralization of cartilage tissue, bone apatite. It is believed that metabolite plays an important role in bone embryogenesis.
Vitamin D is involved in the regulation of the enzyme activity of the head of the head of the Krebs bioenergy cycle, enhances the synthesis citric acid. It is known that citrates are included in the bone tissue.
Vitamin D and its active metabolites affect the cells of the immune system, therefore, with a deficiency of vitamin D, secondary immune failure occurs (the activity of phagocytosis, the synthesis of interleukins 1 and 2, interferon products is reduced.
Neuroendocrine regulation of phosphorous calcium metabolism is carried out by secretion of the parathyroid hormone. Reducing the level of ionized calcium associated with a vitamin D deficiency serves as a signal to increase the level of parathyroid hormone. Under the influence of the parathyroid hormone calcium, bone apatite passes into a soluble form, so that the level of ionized calcium can be restored. The antagonist of the parathyroid hormone is Calcitonin. Under its influence, the content of ionized calcium in blood serum decreases, the processes of bone mineralization are enhanced.
Pathogenesis Rakhita
The process of formation of rickets is complicated and depends on many factors, but primarily from the factors regulating the phosphorus-calcium balance. In a complex picture of the pathogenesis of Rakhita, the reason and the consequence are constantly changing in places, so it is difficult to determine that when rickets are initially, and what is secondary. Conditionally, several stages can be distinguished in the development of the disease.
First stage
Due to the deficiency of vitamin D, the permeability of cell membranes in the intestines changes, which leads to the displacement of calcium suction. In response to hypocalcemia, the activities of parathyroid glasses are activated. Paraptyroid hormone slows down the reabsorption of phosphates in the kidneys. In addition, with a deficiency of vitamin D, the inorganic phosphorus does not split off the organic compounds contained in food. All this leads to a decrease in phosphorus level. Hypophosphatemia is one of the first biochemical manifestations of Rakhita. Calcium level during this period is normal, since the parathyroid hormone enhances the formation of 1, 25-dihydroxycholecalciferol and temporarily increases the resorption of bone tissue, and also at the same time enhances the flow of calcium from the intestine.
Second phase
As calcium deficiency is increasing in the body, not only calcium suction in the intestines is disturbed, but also mobilization of it from the skeleton becomes clearly insufficient, which leads to a decrease in the level of calcium and phosphorus in serum. As a result, the synthesis of the organic matrix of bone tissue, the growth of the bones, their mineralization, develop osteoporosis phenomena (uniform decrease in the volume of bones and other signs) and osteomalysis (bones soften and easily curved). The growth of the defective osteoid tissue may occur due to accumulation in different areas of osteoclasts, since the parathyroid hormone stimulates their education. The activity of alkaline phosphatase produced by osteoclasts increases.
With rickets, the muscle tone is disturbed, which contributes to the occurrence of diffuse richite muscular hypotension. In addition, electrolyte imbalance leads to a violation of the relationship between the sympathetic and parasympathetic regions of vegetative nervous system and the development of vegetative dysfunction.
Third stage
Hypophosphatemia determines the reduction of alkaline reserve of blood and the development of acidosis, which is accompanied by a violation of the exchange of proteins, fats and carbohydrates. There is a decrease in the level of citrates in the blood due to the insufficient formation of the peyrogradic acid in the cycle of tricarboxylic acids. With rickets, not only calcium and phosphorus, but also other microelements (magnesium, potassium, iron, zinc, etc.), is disturbed, therefore Rahit is a disease accompanied by a violation of not only phosphorous calcium, but also all other types of exchange.
Symptoms Rakhita
The first symptoms of Rahita appear already at the age of 1-2 months, and the expanded clinical picture is usually observed at the age of 3-6 months. Initial clinical signs of the disease (sweating, decrease in appetite, resistant red dermographism, increased excitability) arise due to a violation of the functional state of the autonomic nervous system. Soon the dream can worsen, the child begins to turn his head, the "baldness" appears. It is important to emphasize that the detection of only symptoms of the violation of the vegetative nervous system is not a reason for establishing the diagnosis of Rakhit. To make a diagnosis, it is necessary to have changes in the bone system: softening in the course of the cranial seams (craniotabes), soreness when pressed on the bone of the skull, the fuel of the edge of the large springs, the bowl of the head. Due to the osteoid tissue hyperplasia, hypertrophied dark and frontal hypers, "Rachitic kits", thickening of epiphydes of the forearm bones ("Rachitic bracelets") may be formed. With a heavy rickets, you can observe the hanging "Olympic forehead", the smelted bridge. The front of the chest together with the sternum protrudes forward, reminding chicken breasts. The arcuate curvature of the lumbar spine - pathological kyphosis (Rachitic hump) appears. The ribs become soft, puffy, the chest is deformed, the bottom aperture is expanding with the sides, its lower aperture is expanding. At the site of attachment of the diaphragm, Röbeber is appeared - the so-called Garrison Garrison. The hypotension of the muscles of the anterior abdominal wall leads to the formation of a characteristic "frog of the abdomen." In addition to muscle hypotension, the weakness of the ligament apparatus is observed (the breakdown of the joints, the phenomenon of the Gutta-theder boy).
When a child begins to get up, develops O- or X-shaped curvature of the legs (depending on the predominance of the tone of muscle of flexors or extensors).
In patients with Rakhit, the closure of spring and seams later is observed, later teething, dental enamel defects, characterized by the development of early caries.
In addition to bone and muscular disorders, in this case there may be functional changes from the respiratory system (due to the weakness of the respiratory muscles and the deformation of the chest). In some cases, due to severe muscular hypotension, a minor expansion of the boundaries of the heart is possible. The ECG is noted the elongation of QT intervals, Rq, less often - impaired repolarization.
Rachita classification
In Russia, it is customary to use the classification of Rakhita proposed by S.O. Dulitsky (1947). According to this classification, the severity of Rakhit (light, medium, heavy), periods of the disease (initial, gaps, reconstruction, residual phenomena), as well as the nature of the flow (acute, subacute, recurrent) are distinguished. In 1990, E.M. Lukyanova et al. They were offered to add three clinical variants of Rakhit's flow to classification, taking into account the leading mineral deficiency (calcine, phosphorene, without deviations in the content of calcium and inorganic phosphorus in serum).
The severity of Rakhita is assessed taking into account the severity of violations in the bone system, as well as vegetative changes, muscle hypotension, changes in other organs. For rickets, changes in the bone system are characterized against the background of pathological changes in the functional state of the autonomic nervous system. With rickets of the average degree of change in the bone system are more pronounced, muscle hypotension develops. With a serious course of Rakhita, along with severe bone changes and diffuse muscular hypotheses, there is a delay in the development of motor, static functions, as well as the violation of the functions of many internal organs and systems (lung damage, of cardio-vascular system and etc.).
The acute course of Rakhit is most often noted in children of the first half of the life, born with a mass of more than 4 kg, or in children with a large monthly increase. The subacute course of rickets is characteristic of children with intrauterine or postnatal hypotrophy, as well as for premature. With a subacute, Rahute signs of osteoid hyperplasia prevail over signs of osteomalysis, in addition, all the symptoms are developing slower than with acute rickets. For a recurrent rickets, periods of clinical improvement and deterioration are characteristic.
With a calcine variant of Rakhita, children reduced the level of general and ionized calcium in the blood. With the leading role of calcium failure, bone deformations are expressed with the predominance of osteomation processes, increased neuromuscular excitability. In the phosphausenic version of Rakhita, a decrease in the level of inorganic phosphorus in serum is observed. Bone changes are more pronounced due to osteoid hyperplasia, weakness of the ligament. For rickets with minor deviations in the content of calcium and inorganic phosphorus in the blood, a subacute flow, a moderate hyperplasia of osteoid tissue, the absence of implicit changes from the nervous and muscle systems are characteristic.
Diagnostics Rakhita
Laboratory Criteria for Active Rachita
- reducing the content of inorganic phosphates in blood serum to 0.6-0.8 mmol / l;
- reducing the concentration of total calcium in the blood to 2.0 mmol / l;
- reducing the content of ionized calcium less than 1.0 mmol / l;
- an increase in the activity of alkaline phosphatase in serum of 1.5-2.0 times;
- reducing the content of 25-hydroxycholecalciferol in serum of blood to 20 ng / ml and below;
- reducing the level 1, 25-dihydroxycholecalciferol in serum to 10-15 pg / ml;
- compensated metabolic hyperchlorinemic acidosis with base deficit to 5.0-10.0 mmol / l.
Rachita radiological criteria
On radiographs, the disruption of bone mineralization is manifested by the following signs:
- changes in the clarity of the boundaries between the epiphysis and metaphy (that is, in the zones of the preliminary observation, the boundary becomes uneven, blurred, fringe);
- progressive osteoporosis in places of maximum bone growth, increasing distance between epiphysis and diaphysia due to increasing metaphysis;
- disruption of contours and the structure of epiphysis ("Swuffling epiphysses"). X-ray signs in the process of developing the disease are changed.
Differential diagnosis of rickets are carried out with other diseases having similar clinical symptoms: renal tubular acidosis, vitamin D-dependent rickets, phosphate-diabetes, Debre de Tony-Fanconi disease, hypophosphate, cystinosis.
Treatment Rakhita
The treatment of Rahita must be comprehensive, the prescription of therapeutic doses of vitamin D, as well as the use of medical and recreational activities. Depending on the severity, therapeutic doses of vitamin D are 2000-5000 IU / day for 30-45 days. At the beginning of treatment, vitamin D is prescribed in a minimum dose - 2000 IU for 3-5 days, with good tolerability, the dose is raised to an individual healing dose. After achieving the therapeutic effect, the therapeutic dose is replaced by preventive (400-500 IU / day), which the child receives during the first 2 years of life and in the winter period in the third year of life.
For the treatment and prevention of Rakhita for many years, vitamin D preparations (Ergocalciferol or cholecalciferol solutions) are used. Forms of release many medicinal preparations Call certain problems due to the complexity of the dosing. So, in recent years, the alcohol solution of vitamin D2 is practically not released due to the danger of its overdose. For the treatment and prevention of Rakhitol, a whitate can be used - an oil solution of vitamin D3 (in one drop - 600 IU) and domestic oily solutions of vitamin D2 (in one drop - 700 IU). However, the oil forms of vitamin D are not always well absorbed, therefore, in the syndrome of impaired intestinal suction (celiac disease, exudative enteropathy, etc.), vitamin D oil solutions are used limited. In recent years, the prevention and treatment of Rahita is widely used by the water form of vitamin D3 - aqualeber, having a pre-adequate dosage form for receiving and clear dosage. One drop of a solution of cholecalciferol (aquadeurim) contains 500 vitamin D3. The advantage of aqueous solution is rapid suction from the digestive tract. The solution is well absorbed and does not cause dyspeptic disorders.
In the presence of patients with rakhita children of accompanying acute diseases (ORVI, pneumonia, etc.) vitamin D should be canceled for a period of high temperature (2-3 days), and then appoint again in the medical dose.
In addition to vitamin D, calcium preparations are prescribed in the treatment of Rakhita: calcium calcium glyceluchosphate (0.05-0.1 g / day), calcium gluconate (0.25-0.75 g / day) and others. To increase calcium absorption in the intestine, prescribe Citrate mixture, lemon juice or grapefruit juice. To normalize the function of the central and vegetative nervous system, magnesium and potassium aspargincture (asparks, Panangin), as well as glycine are prescribed. If rickets leaks against the background of hypotrophy, a 20% aqueous solution of carnitine (chloride carnitine) can be prescribed from the calculation of 50 mg / (kgxut) for 20-30 days. Chloride carnitine contributes to the normalization of metabolic processes, the indicators are improved under its influence physical development. In addition, it is possible to use orottic acid (orotat potassium) from the calculation of 20 mg / (kgxut). It is known that ocheric acid enhances the synthesis of calcium-binding protein in the intestine enterocytes. Of particular importance is the use of antioxidants: acetate tocopherol (vitamin D) in combination with ascorbic acid (vitamin D), glutamic acid, beta-carotene. After 2 weeks from the beginning of drug therapy, the treatment of physical education and massage are added to the complex of therapeutic measures. After graduating from drug treatment, children are older than six months medical baths (salt, coniferous).
Prevention Rakhita
Distinguish the antenatal and postnatal prevention. It can be nonspecific and specific (using vitamin D).
Antenatal prevention Rakhita
The antenatal prevention of Rakhita begins before the roe of the child. With the patronage of pregnant women draw the attention of the future mother to comply with the routine of the day, sufficient stay in the fresh air, for rational food. Pregnant women should eat at least 200 g of meat, 100 g of fish, 150 g of cottage cheese, 30 g of cheese, 0.5 l of milk or kefir, fruits, vegetables. In the last 2 months of pregnancy, a woman should receive vitamin D daily 500 IU, in the autumn-winter period - 1000 meters. Pregnant women from risk groups (nephropathy, chronic extragnenital pathology, diabetes, hypertensive disease) It is necessary from the 28-32nd pregnancy week to appoint vitamin D at a dose of 1000-1500 me.
Forecast with Rakhita
With the early diagnosis of rickets and the appropriate treatment, the disease is favorable and without consequences. Without treatment, Rahit is an average and severe degree may adversely affect the subsequent development of children. There are compassion and deformation of the pelvis, flatfoot, myopia, a multiple dental damage (caries) may appear. Breast-age children suffering from rickets are subject to frequent acute respiratory diseases, pneumonias, etc.
Under the dispensary observation (quarterly inspection) for 3 years there must be children, transferred to the average and heavy rickets. Specific prophylaxis are carried out during the second year of life in the autumn, winter and spring periods, and on the third year of life - only in the winter.
With rickets, vaccinations are not contraindicated. Planned prophylactic vaccination can be made 2 weeks after the appointment of vitamin D.
Bibliography
Korovina H.A. et al. Prevention and treatment of rickets in children (lecture for doctors) / H.A. Korovina, A.B. Cheburkin, I.N. Zakharov. - M., 1998. -28 p.
Novikov P.V. Rahit and hereditary ricket-like diseases in children. - M., 2006. - 336 p.
Novikov P.V., Kazi-Akhmetov E.A., Safonov A.V. New (water-soluble) Vitamin D form for the treatment of children with vitamin D-deficient and hereditary D-resistant rickets // Russian Bulletin of Perinatology and Pediatrics. - 1997. - № 6. - P. 56-59.
Prevention and treatment of rickets in young children: Guidelines / Ed. EAT. Lukyanova et al. - M.: M3 of the USSR, 1990. - 34 p.
Stops V.I. Rahit in premature babies (lecture for doctors). - Penza, 1990. - P. 29.
Fox A.T., Du Toil G., Lang A., Lack G. Food Allergy As A Risk Factor for Nutritional Rickets // Pediatr Allergy Immunol. - 2004. - Vol. 15 (6). - P. 566-569.
Pettiforj.m. NUTRITIONAL RICKETS: DEFICIENCY OF VITAMIN D, CALCIUM OR BOTH? // AM. J. Clin. NUTR. - 2004. - Vol. 80 (6 Suppl.). - P. i725SH729S.
Robinson p.d., Hogler W., Craig M.E. et al. The Reemerging Burden of Rickets: A Decade of Experience from Sidney // Arch. DIS. Child. - 2005. - Vol. 90 (6). - P. 1203-1204.
Zaprudnov A.M., Grigoriev K.I. Rahit in children. - M., 1997. - 58 p.
It's important to know!
Vitamin D-dependent Rahit. This group includes two diseases with autosomal-recessive inheritance. With the first type of dependence on vitamin D, there are mutations of the gene (12th pair of chromosomes), which is responsible for the synthesis of 1a-hydroxylase in the kidneys, as a result of which the deficit of active metabolite D is arising.
Information: RICKETS. Etiology. One of the main factors is hypovitaminosis D, vitamin D deficiency of exogenous or endogenous origin. In addition to the wrong feeding and alimentary insufficiency of vitamin D, it can lead to a violation of the formation of its active forms in the body with a lack of ultraviolet rays (in winter and autumn, in cities), liver and kidney disease (they are formation of active forms of vitamin). A certain role is played by presence (immaturity of enzyme systems), the rapid growth of the child, diseases accompanied by acidosis, the insufficient flow of calcium and phosphorus salts. Pathogenesis. Vitamin D is a steroid compound and is known in the form of vitamin D2 (ergocalciferol) and vitamin D3 (cholecalciferol), which are very close in structure, physicochemical properties and influence on the human body. The vitamin D coming with food is transformed into liver and kidneys, resulting in 1.25-dihydroxy-vitamin D, which has a hormone-like action. This compound affects the genetic apparatus of the intestinal cells, thereby increasing the synthesis of protein, specifically binding calcium and providing its transport in the body. With a lack of vitamin D, the absorption and exchange of calcium is disrupted, its blood concentration falls, which causes the reaction of the parachitoid glands and increase the secretion of the pararathgamon regulating the exchange of calcium and phosphorus. The over-secretion of the parathgamon leads to mobilization of calcium from bone tissue, suppressing phosphate reabsorption in renal channels, and therefore the content of inorganic phosphates in the blood drops. At the same time, alkaline phosphatase activity sharply increases. The phosphate-calcium exchange disorders lead to the development of acidosis, which is accompanied by a violation of the excitability of the nervous system. Clinical picture. In gravity, the following degrees of Rahita distinguish: 1 degree (light) - small changes from the nervous and muscle systems; residual phenomena does not give; II degree (moderate severity) - pronounced changes in bone, muscular, nervous and hematopoietic systems, moderate disruption of the function of the internal organs, a slight increase in the size of the liver and spleen, anemia; III degree (severe) - sharply pronounced changes from the central nervous, bone and muscular systems, internal organs. Frequent complications. The initial period is more often noted in 2-3 months, but can manifest itself throughout the first year of life. Sweating, baldness of the head, anxiety, muscular dystonia; The unaware softening of the edges of a large springs. Duration 2-3 weeks. Biochemical studies: a reduced amount of phosphorus, an increase in phosphatase activity. No radiographic changes. In the period of sickness of the disease, along with the phenomena of braking the nervous system, changes in the bones appear; Craniotabes, changes in the bones of the skull, chest, limbs. The bone changes, unobthered with rickets) degrees and distinct at the II degree, are transferred to deformation with rickets of III degree. Disruption of static functions, internal organ functions, muscle hypotension, anemia is joined. When Rahute II and III degrees of the spleen and the liver are increased. On radiographs, the contours of bones are lubricated. Epiphysis of tubular bones of glassoid, edges of metaphistes are fringeless. On the 2-3rd year of life there are only consequences in the form of bone deformations, sometimes anemia. In acute flow, the rashita symptoms are noted. In the initial period - severe concern, sharp sweating, biochemical shifts in the blood, in the midst of the disease, a significant softening of bones, pronounced muscle hypotension. The acute course is observed more often in the first months of life, especially in premature and rapidly growing children. The subacute flow is characterized by a slower development of the process. It is observed more often in children over 6-9 months, as well as in children with hypotrophy. The phenomena of softening bones are expressed significantly less. Osteoid hyperplasia prevails over osteomation, frontal and dark bugs, rosary on ribs, thickening of epiphesis of tubular bones are noted. The recurrent flow is accompanied by intermittent states: usually improving summer and worsening in winter. Radiographs are visible on radiographs that correspond to observation zones in metaphyshs during the reparation. Late Rickets include rare cases of the disease, when active manifestations are noted over the age of 4. Late Rahit, observed in the military and the first postwar years, was characterized by the presence of general symptoms of the disease (anorexia, sweating, pain in the legs, fatigue). Bone deformations are marked only in terms of cases. Of particular importance are such signs as hypophosphatemia, and from the bones - osteoporosis and changes in occasion zones. The diagnosis in addition to clinical symptoms is confirmed by the study of the blood content of calcium, phosphorus, alkaline phosphatase, the data of x-ray research is important. Differential diagnosis. Rachitis differentiate from a number of ricket-like diseases of hereditary natural phosphate-diabetes, renal tubular acidosis, Debre's syndrome - de Tony Fanconi (see ), as well as from the congenital dislocation of hips, hondodroodstrophy, osteopathy in chronic renal failure, congenital bone fragility. Treatment. An important role is played by rational nutrition, normalization of a regime with sufficient stay in the fresh air, massage, gymnastics. In the initial manifestations of docking children prescribe vitamin D2 preparations of 300-800 IU / day, for the rate of 400,000-600,000 me; During the ranking period, 10,000-16,000 IU / day are prescribed in 2-3 receptions, for a course of 600,000-800,000 ME. The impact dose method used in severe complicated formas of rickets is currently not used. Vitamin D drugs should be given during meals. Sometimes the purpose of vitamin D2 is combined with a 25% solution of citric acid, a 20% sodium citrate solution (in the intestine, an easily soluble and well suused calcium citrate complex is formed) inside 20 ml per day. During treatment, you need to implement the simplest sensitivity control. children's body To vitamin D using Sulkovich sample for the prevention of hypervitaminosis. Ultraviolet therapy has a beneficial effect in the initial period and at a subacute of Rahita in young children. The method and dosage of irradiation depend on the age of the child, its physical condition, the conditions of the external environment, phase and the severity of Rakhita. It is recommended to carry out ultraviolet irradiation with a course, including 15-20 sessions appointed in a day, with a gradual increase in exposure. The first session of children up to 3 months begin with 1/8 biodozes, children over 3 months - with 1/4 biodoz. With subsequent treatment, after each 2 session, the exposure is increased by 1/8, or 1/4 biodoz. With insufficient stay in the open air, artificial feeding, the recurrent course of Rakhit, the course of treatment is lengthened to 25 sessions and repeated after 2 months. With the initial phase of Rakhita, irradiation is often limited to one course consisting of 15-20 sessions, in the middle phase, the course after 2-3 months increases. In the intervals between irradiation courses, specific prevention of vitamin D2 or fish oil are carried out. Massage and gymnastics are used in any period, but not in acute flow. The forecast for the timely treatment and elimination of the cause is favorable. With severe flow, psychomotor development delay, skeletal deformation and posture disturbance. Prevention. Rational nutrition, sufficient insolation, sanitary and hygienic regime, hardening, proper education. Advocative antenatal prevention in pregnant women in the last 2-3 months of pregnancy vitamin D, 5,500-1000 me / day. For the antenatal prevention, you can use ultraviolet irradiation of pregnant women. It is necessary for a long stay outdoors, rational food. In the diet of the child, vegetables, fruits should be in time. The lore must contain a sufficient amount of vitamins, salts. Important products containing natural vitamin D3 (egg yolk, fish oil) are important. The addition of a citric acid is artificially fed to nutrition (25% solution of 1 teaspoon 3 times a day) contributes to the formation of an easily absorbed Citrate calcium, and therefore the absorption of phosphorus. Flour dishes, porridges contain phosphorus in a poorly digestible child form and can contribute to the development of rickets, so it is desirable that the number of them in the daily diet of the child of the 1st year of life exceeded 180-200 g. In the autumn-winter period, ultraviolet radiation of children with preventive goal It is necessary to start with 1-1.5 months of life. Two courses should be held with intervals 2 months. The physiological need for a vitamin D of a healthy ditching child in the 1st year of life ranges within 400-500 IU / day. In cases where the child for any reason does not receive ultraviolet irradiation with the preventive purpose, the artificial drug of vitamin D2 or D3 should be prescribed for the purpose of the antenatal prophylaxis in the last 3-4 months of pregnancy, gendests are recommended for 1-2 dragey per day (250- 500 ME vitamin D2), a under adverse conditions - 4 dragey per day. Contraindications - Mother's age for over 30 years, Mother's disease. Postnatal prevention is carried out from a 2-3-non-sex age of 500 me per day (1 drop of video khol), for course 150,000-200 000 ME.
RCRZ (Republican Center for Health Development MD RK)
Version: Clinical Protocols MOR RK - 2014
Valgus deformation, not classified in other categories (M21.0), Varetle deformation, not classified in other categories (M21.1), other congenital bone-muscular deformations (Q68), other disorders due to dysnywent dysfunction (N25.8) Other refined acquired limb deformations (M21.8), phosphorus metabolic disorders (E83.3), the consequences of Rakhit (E64.3), the acquired deformation of the limbs is unspecified (M21.9)
Pediatrics, traumatology and children's orthopedics
general information
Short description
Expert Council of RSA on PVV "Republican Center for Health Development"
Ministry of Health I. social Development Republic of Kazakhstan
Rickets - Systemic disease, as a rule, early children, the basis of which is a violation of calcium and phosphorus exchange. Cost formation dissemination, the functions of the nervous system and internal organs suffer.
Rachi-like diseases belong to the skeleton hondodistrophi group associated with the violation of the functions of the kidneys or intestines.
I. Introductory part
Protocol name: The consequences of Rakhita
Protocol code:
Codes on the ICD 10:
E64.3 The consequences of Rachita
E83.3 Phosphorus Violations
N25.8 Other disorders due to dysnyati dysfunction
M21.0 Valgus deformation not classified in other categories
M21.1 Varetle deformation, not classified in other categories
M21.8 Other refined acquired limb deformations
M21.9 Acquired Limgus Deformation Unspecified
Q68 Other congenital bone-muscular deformations
Abbreviations used in the protocol:
HIV - human immunodeficiency virus;
With a general practice doctor;
ELISA - an immunoassay analysis;
CT - Computer Tomography
LFK physiotherapy
Many - international normalized relationship;
OAK - a general blood test;
OAM - general urine analysis;
UFO - ultraviolet irradiation
Shchychochny phosphatase
ECG - electrocardiography
Protocol development date: year 2014.
Protocol users: Children's orthopedic traumatologists, children's surgeons, pediatricians, medical rehabilitologists (physiotherapists, physiotherapy physical physiography), general practitioners.
Classification
Clinical classification
Under the disease period:
Elementary;
Height;
Reconvation of residual phenomena.
By the nature of the flow:
Acute;
Subacute;
Recurrent.
According to the degree of deformation:
1 degree light (curvature in the frontal plane from 5-15º)
2 degree of average (15-30º);
3 Heavy degree (30-55º).
By type:
Vitamin D-resistant Rahit;
Rahit in renal chronic insufficiency;
Rachet with kidney tubular disorders.
Diagnostics
II. Methods, approaches and diagnostic and treatment procedures
List of basic and additional diagnostic events
Main (mandatory) diagnostic surveys conducted on an outpatient level:
Radiography of both limbs in 2 projections.
11.2 Additional diagnostic surveys conducted on an outpatient level:
Biochemical blood test (phosphorus, potassium, schf, calcium);
CT lower extremities (to clarify the nature of violation and solve the issue of testimony for surgical treatment);
The minimum list of the survey, which must be carried out in the direction of the planned hospitalization:
Determination of blood type;
Determination of the reserves of the factor;
General urine analysis;
Coagulogram (the duration of bleeding and time of coagulation, protontine, fibrinogen, adhesion response and platelet aggregation, antithrombin);
Main (mandatory) diagnostic surveys conducted at the stationary level:
Determination of blood type;
Determination of the reserves of the factor;
Radiography of the limbs in 2 projections in order to control in dynamics.
Additional diagnostic surveys conducted at the stationary level:
General urine analysis;
Coagulogram (the duration of bleeding and coagulation time, protuberine, fibrinogen, adhesion reaction and platelet aggregation,
Antithrombin);
Biochemical blood test (general protein, alanineanotransferase, general cholesterol, bilirubin, direct bilirubin, creatinine, urea, glucose, potassium, sodium, phosphorus, calcium, chlorine);
CT lower extremities (to clarify the nature of violations and solve the issue of testimony for surgical treatment).
Diagnostic measures carried out at the ambulance stage: are not conducted.
Diagnostic criteria
Complaints and anamnesis
Complaints on the :
Progressive deformations of the limbs causing a cosmetic defect, oppressing the psychological status of the patient;
Fast fatigue;
Pain in the limbs;
Breach of gait;
Loge in growth.
Anamnesis :
Diseases are more often manifested soon after birth or in the first three years of life;
Frequent respiratory diseases;
The progression and degree of deformation depends on the type and form of the disease of the lower limb, occurs more often from the age of 7 months to 3 years.
Physical examination:
Identification of Valgus or Varetle deformations of the lower extremities, the deformation of the chest ("Rachitical rosary"), thickening of the distal departments of the forearm ("bracelets").
Laboratory research:
Blood chemistry: Reduced phosphate, improving the level of SFF.
General urine analysis: increased the release of phosphates, there may be an increase in glucose in the urine, Kaliuria.
Tools:
Chest research x-ray: Osteoporosis, expansion of metaphysis and epiphesis and irregularity of their distal contours, increases the distance between the osening kernels. In case of Erlahra-Blunt, the curvature of the tibia at the level of the proximal department of metaphiz, which is determined in the form of a beak bone protrusion. The deformation of the epiphyse, the inner part of its articular surface is located space, at an angle of 30 - 45gr in the distal direction, the internal epiphyse department is reduced in height almost 2 to 3 times, it is possible to edge fragmentation.
CT research of lower extremities: Determines the nature of the deformation of the epimetaphyphizar bones, the state of the joint surfaces, the form of plateau and thes of the femoral and tibia, the state of the fizar plate (expansion, uzuration, narrowing, expansion, synostotesia), the structure of bone tissue; .
Indications for consulting narrow specialists :
Consultation of pediatrician / nop (with a concomitant somatic pathology);
Surgeon consultation;
Consultations of the oncologist (in the presence of the formations of the bone skeleton to eliminate malignant formations);
Consultation of the phthisiatra (to eliminate bone tuberculosis);
Consultation of the cardiologist (with pain in the heart of the heart and the availability of changes to the ECG);
Consultation of the psychologist (if there are changes in psychological status);
Consultation of genetics (in the presence of hereditary agarial factors and diseases);
Consultation of the endocrinologist (in the presence of concomitant endocrine pathology);
Consultation of a medical rehabilitologist (for the appointment of early rehabilitation treatment);
Consultation of a transfusion physician (if there is indications for the purpose of intravenous transfusions);
Consultation of the otorinolaryngologist (in order to identify and rehabilitate chronic foci of infection);
Consultation of the dentist (in order to identify and sanitation of chronic foci of infection).
Differential diagnosis
Differential diagnosis of the consequences of Rakhita
|
Signs |
The consequence of Rakhita | Rachi-like diseases | Erlacher Blunt Disease |
| Manifestation of deformation of the lower limb | From 7-8 months to 2 years, the period of residual phenomena is observed from 2-3 years | In the first two years of life, maybe to youthful age |
Infantile Form: 2.5-3 years Juvenile form 7-8 years old |
| Signs detected by radiation diagnostic methods | The deformations of the lower extremities are observed after 3 -5 years and the nature of the varestic or valgus. | The bone changes, characteristic and similar to those with ordinary rickets, are detected: the expansion of the ends of tubular bones, metaphyshes have boil-shaped thickening, expansion epiphyseal zones have uneven blurred contours. At the level of the osteoporosis zone, alternate with osteosclerosis zones. | The curvature of the tibia at the level of the proximal department of metaphiz, often near the border with the epiphysis, which is determined in the form of a beak-like bone protrusion. The inner part of the epiphyse is located at an angle of 30 -45 gr in the distal direction, reduced height, possibly edge fragmentation. |
Treatment abroad
Treat treatment in Korea, Israel, Germany, USA
Get advice on medical examination
Treatment
Purpose of treatment:
Elimination of limb deformation;
Eliminating a cosmetic defect and improving the quality of the patient's life.
Tactics of treatment
Non-drug treatment:
Diet: Table number 15.
Mode: Common.
Medicia treatment
Antibacterial therapy:
in order to prevent postoperative complications:
. 1 generation cephalosporins: Cephazoline, 50-100 mg / kg, intravenously, one-time 30-60 minutes before the operation.
. cephalosporins 2 and 3 generations:
Cefuroxime, 50-100 mg / kg / day, in 3-4 administration; intramuscular or intravenously;
Or ceftriaxone, 20-75 mg / kg / day, in 1-2 administration, intramuscular or intravenously;
Or cefapanceraxone, 50-100 mg / kg / day, in 2-3 administration, intramuscularly or intravenously;
. lincoosamids:
Lincomycin
Intramuscularly, 10 mg / kg / day, every 12 hours,
Intravenous drip administration at a dose of 10-20 mg / kg / day, in one or more administrations with severe infections and children from 1 month and older;
. glycopeptides:
Vancomycin: 15 mg / kg / day., Not more than 2 g / day., Every 8 hours, intravenously, each dose should be administered at least 60 minutes.
Package therapy (in the postoperative period):
nonarcotic analgesics:
. paracetamol, 200 mg, Tablets - at the rate of 60 mg per 1 kg of body weight of the child, 3-4 times a day. The interval between the techniques should be at least 4 hours. Maximum daily dose 1.5 g - 2.0 g;
Paracetamol Suppositories Rectal 125, 250 mg - one-time dose is 10-15 mg / kg of the body weight of the child, 2-3 times a day, after 4-6 hours;
Paracetamol suspension 120 mg / 5 ml, for intake - a single dose of the drug is 10-15 mg / kg of body weight, 4 times a day, the interval between each reception is at least 4 hours (dose for children aged 1 to 3 Mon. Determined individually).
Paracetamol syrup for intakes of 2.4% 50 ml - children from 3 to 12 months to ½ -1 teaspoon (60 -120 mg); from 1 to 6 years 1-2 teaspoon (120-240 mg); From 6 years to 14 years old 2-3 teaspoons (240-360 mg), 2 - 3 times a day.
The maximum duration of paracetamol treatment with no more than 3 days as analgesics.
. suspension of ibuprofen 100 mg / 5ml - 200 ml, for intake, 7-10 mg / kg body weight, maximum daily dose - 30 mg / kg. The interval between the drugs should not be less than 6 hours. The duration of treatment is no more than 5 days, as an anesthetics.
opioid analgesics:
. tramadol 50 mg / ml -2 ml in the solution for injections,
Children from 1 to 14 years old: from 1 mg / kg to 2 mg / kg Weight intravenously, intramuscularly or subcutaneously. Intravenous injections should be introduced very
Slowly or they should be divorced in infusion mortar and administered by infusion. The dose can be repeated with an interval of 4-6 hours.
. trimeperidine 2% -1 ml in solution for injection, children over 2 years old, dosage is 0.1 - 0.5 mg / kg body weight. It is contraindicated to children up to 2 years.
. morphine 2% 1 ml:
From 2 to 3 years old, a single dose is 0.1 ml (1 mg of morphine), daily - 0.2 ml (2 mg of morphine);
3-4 years: one-time dose - 0.15 ml (1.5 mg), daily - 0.3 ml (3 mg);
5-6 years: one-time dose - 0.25 ml (2.5 mg), daily - 0.75 ml (7.5 mg);
7-9 years: one-time dose - 0.3 ml (3 mg), daily - 1 ml (10 mg);
10-14 years: one-time dose 0.3-0.5 ml (3-5 mg), daily - 1-1.5 ml (10-15 mg).
Infusion therapy with crystalloid solutions For the purpose of replacement and correction of water and electrolyte exchange:
. sodium chloride solution 0.9% - introduced 20-30 ml / kg;
. dextrose 5% - On the first day, 6 g of glucose / kg / day are introduced., Subsequently - up to 15g / kg / day.
Blood preparations With a substitution goal, depending on the perioperative blood loss:
. freshly frozen plasma (with a shortage of circulating blood volume more than 25-30%, due to blood loss, with a plasma of more than 1.5 (norm 0.7-1.0), transfusion intravenously at a dose of 10-20 ml / kg of mass);
. erythrocyte suspension (With a shortage of circulating blood volume more than 25-30%, hematocrit is less than 24%, reduced hemoglobin below 70-80 g / l, due to blood loss, the occurrence of circulatory disorders shows a transfusion in a dose of 10-20 ml / kg of body weight.
. thromboconcentrat (With a decrease in platelet levels below 50 * 10/9, on the background of bleeding, with further maintenance of platelet levels 100 * 10/9 - transfusion intravenously 1 dose by 10 kg of mass).
Medical treatment rendered on an outpatient level:
Correction of the underlying disease under the supervision of pediatrician and children's endocrinologist.
Medical treatment provided at the stationary level
List of basic medicines
(having 100% probabilities):
Antibiotics:
Cephazoline 500 mg powder for the preparation of a solution for intravenous and intramuscular administration
Non-Steroid Protection Facilities:
Paracetamol, 200 mg tablets;
Paracetamol, rectal suppositories 125, 250 mg;
Paracetamol suspension for reception inside 120 mg / 5 ml;
Paracetamol Syrup for intakes inward 2.4% 50 ml;
Ibuprofen, suspension for reception inside 100 mg / 5ml-blcon 200 ml with a syringe dosing.
Analgesic:
Tramadol - 50 mg / ml -1 ml injection solution;
Trimepyridine - 1 or 2% - 1 ml injection solution;
Morphine is 1% - 1 ml, an injection solution.
Plasmoving and perfusion solutions:
Sodium chloride 0.9% - 500, 400, 200 ml solution for intravenous infusion (50%);
Dextrose 5% - 500, 400, 200 ml solution for intravenous infusion (50%).
List of additional drugs (less than 100% probability):
Antibiotics:
Cefuroxime, powder for preparing the solution for injection and infusion 750mg and 1.5G;
Ceftriaxone, powder for the preparation of the solution for injections of 0.5 g and 1.0 g.;
Cefapancerone, powder for the preparation of solution for intravenous and intramuscular administration 1.0 g.;
Lincomycin, solution for intravenous and intramuscular administration, 300 mg / ml.;
Vancomycin, lyophilisate for the preparation of the solution for infusions, 500 mg, 1000 mg.
Medical treatment provided at the ambulance phase: not carried out.
Other types of treatment:
Other types of treatments rendered on an outpatient level:
Massage,
Physiology;
The imposition of plumbing gypsum bandages in order to conservative correction of deformations;
Wearing orthoses and tires.
Other species rendered at the stationary level:
Inhalation;
Physiology;
Simulators
Other types of treatment rendered at the stage of ambulance: not carried out.
Surgical intervention
Surgical intervention rendered on outpatient conditions: not carried out.
Surgical intervention provided in stationary conditions
Types of operations :
Correcting osteotomy limbs at the place of deformations with various species fixation (spokes, screws, coarse and intramedullary osteosynthesis, incolda of the Ilizarov apparatus), in some cases according to the use of auto and alomethers;
Temporary epiphysiodesis;
Operations (prolonged directional self-correction) of the varestic deformation of the limb - the temporary epiphysiodesis of the distal ends of the femur and proximal ends of the tibial bones.;
Removal of metal structures of the upper limb;
Dismantling of the apparatus through bone osteosynthesis of the upper limb.
Indications for the operation (Availability 2 or lower listed criteria):
Deformation of the lower extremities 1-3 degrees;
Availability of complaints;
Progression of deformation;
The presence of metal structures.
Absolute contraindications to surgery:
The presence of chronic concomitant diseases in the decompensation stage (heart, kidneys, liver, etc.);
Mental disorders, inadequate patient.
