Rickets in infants: photos, symptoms, treatment and prevention of the most common disease in infants. Rickets: symptoms of the disease Rickets in infants 1 degree what to do

Update: October 2018

In the list of diseases of infancy, a violation of phosphorus-calcium metabolism, called rickets, takes an honorable second place. The risk group for the onset of rickets is more than half of children under the age of 2 years.

A typical rickets is a child from six months to a year and a half, or with a large weight, living in an industrial city in northern latitudes, often ill and being bottle-fed.

Rickets in infants is a common cause of developmental delays and malfunctions in the immune system.

Where does vitamin D come from

About seven variations of vitamin D are known. They enter the body with food or are synthesized in the skin. The most active vitamin D2 (ergocalciferol), contained in plant foods, and D3 (cholecalciferol), supplied with animal food.

In the skin, when exposed to ultraviolet light, provitamin D3 is converted into vitamin D3. After the vitamin is synthesized or absorbed in the intestines, part of it is deposited in the adipose tissue of the muscles, and the other is transferred to the liver.

In the kidneys and liver, the inactive form of the vitamin undergoes hydroxylation processes and is converted into active metabolites. In the liver, this is aided by the enzyme 25-hydroxylase, and in the kidneys by 1-alpha-hydroxylase. The result is the formation of calcidiol in the liver. And in the kidneys - calcitriol.

How does vitamin D work

• Provides absorption of calcium by the intestinal wall
• Enhances the reuptake of calcium and phosphorus by the renal tubules
• Accelerates the impregnation of bone tissue with mineral salts
• Works as an immunomodulator
• Stimulates the exchange of tricarboxylic acids

How Risk Factors Work

• premature babies- A newborn who was not lucky enough to be born prematurely has a lot of errors in the enzymatic systems, which makes it difficult for the absorption of vitamin D even with normal feeding.
• big baby- requires large amounts of vitamin than its peers.
• Artificial - receives nutrition in which the phosphorus-calcium ratio differs from that in breast milk and makes it difficult to absorb these minerals.

In the infant period, the child's body is not mature enough to normalize all types of metabolism, even in conditions where there is no hypovitaminosis.

In addition, during this period of time, a child living in a harsh climate wraps up more, even in the warm season (because he is not hardened), less often in the air without clothes and hats. Even the pitiful amounts of ultraviolet insolation that he could receive are ignored due to the risk of colds and ear infections.

In the same period, dysbiosis phenomena are frequent, which disrupt absorption and enzymatic processes, which affects the metabolism of the vitamin. Also, due to problems with the intestines, the child is on a sparing feeding regimen for a longer period of time, later receives complementary foods, which limits the natural intake of the vitamin from food (see).

Frequent respiratory diseases lead to an increase in the need for the vitamin, as well as impair its absorption, shorten the frequency and time of walking.

Despite all of the above, it was noted that among the peoples of the Far North or North American Indians, leading a traditional way of life, children practically did not suffer from rickets on such a scale as is observed in modern residents of large cities in northern latitudes.

The thing is that the children of these peoples practically from birth were on the street for most of the day, fed on mother's milk until the age of two or three years and did not constantly suffer from respiratory infections, like the modern generation.

At the same time, in industrialized Great Britain, even at the beginning of the 20th century, children in cities not only got sick, but also died en masse from rickets, for which the disease was nicknamed “English”.

There is also a genetic predisposition to rickets (based on the characteristics of enzymatic systems) in the Negroid race.

Recent studies by specialists prove that there is a hereditary nature of the disease, when, in the absence of vitamin D deficiency, in some variants of the course, a gene mutation is detected. It is assumed that children with the 2nd blood group and mostly boys are more susceptible to rickets, girls get sick in a milder form. At risk are overweight and premature babies. Vitamin D deficiency is considered the main cause of rickets - due to a small amount of it in food, disruption of the digestive tract, poor formation of vitamin D in the skin due to lack of ultraviolet radiation.

How is rickets classified?

There is a primary form of the disease associated with a deficiency in the intake or synthesis of vitamin D and a secondary one.

Secondary rickets is observed when:

• malabsorption
• with renal pathologies
• with diseases of the biliary tract
• with fermentopathy
• with long-term use of anticonvulsants
• with insensitivity of receptors to vitamin

According to disorders of calcium and phosphorus metabolism, rickets is divided into:

• calcium deficient
• phosphorus deficient
• without errors in the level of calcium and phosphorus

According to the nature of the course of the disease, they are distinguished:

• acute rickets with a predominance of rarefaction of bone tissue
• subacute, when bone growth predominates over rarefaction
• recurrent rickets is characterized by the presence of signs of an active process and previously transferred rickets

Symptoms of rickets in children under one year old

The stages of rickets in infants are divided into the period of initial manifestations, the peak, and the period of residual effects.

Initial manifestations

They fall on the age of 3-4 months in infants. Less commonly, the first manifestations of rickets in infants are observed at 2 months or six months. There was a connection between the onset of the disease and rapid weight gain or an infectious disease (including SARS). The duration of this period is about 4 weeks.

• Most often, the debut of rickets, noted by parents, is manifested by an increase in the sweating of the child, especially his head. When a child sleeps, his pillow may be quite wet. Similar sweating is observed during periods of activity of the child (eating, breastfeeding, games).
• The second frequently noted symptom is the gradual baldness of the back of the head in children under one year old and their increased reaction to noise. If earlier the child did not react to the usual household noises, now he wakes up or shudders from any sound.
• But in addition to the symptoms that are noticeable even to a non-specialist, in the initial period of rickets there is a significant softening of the bone tissue. The edges of the large fontanel, the sternocostal joints become soft, the formation of tubular bones slows down.

The height of the disease

This period is characterized by increased bone formation. At the same time, persistent bone deformities and disturbances in the functioning of the nervous system appear. Internal organs, hematopoietic system. There are three degrees of severity of rickets. which can be distinguished precisely in this period (light, medium and heavy).

• Bone deformities

They come down to the curvature of the clavicles, lower legs (o-shaped or x-shaped deformation). Bone outgrowths (rachitic rosaries) form on the wrists, cycolottes and sternoclavicular joints. An impression or excessive bulge of the sternum, a transverse groove of the chest (Harrison's groove) is formed. The head acquires an angular shape, the forehead becomes abnormally convex, the hard palate and jaw arches are deformed. Teeth erupt unevenly and with a delay (see).

• Decreased muscle tone

This affects motor delays and the failure of normal motor activity. The child begins to lag behind in terms of turning over, sitting, standing. He develops poor posture and hypermobility of the joints. He is more prone to domestic injuries.

• The nervous system suffers significantly

From the side of the central nervous system, there is an increase in excitability, irritability. Sleep is disturbed. Higher cortical functions suffer: the child learns worse, loses already acquired skills. The autonomic system responds to rickets with red dermographism. Violation in the regulation of the work of internal organs.

• Decreased appetite

The most unpleasant manifestation may be the rejection of the breast or mixture. The child refuses to eat, and no lengthening of the intervals between feedings helps the cause. It affects muscle lethargy, an increase in anemic oxygen starvation and a decrease in the production of digestive enzymes.

• most pronounced in the anemic variant of rickets. The child is pale, easily tired, lethargic, drowsy.
• The immune system is weakened, and the risks of various acute diseases increase.

Signs of rickets in a child may include:

1. Dwarfism
2. Craniotabes - thinning and softening in the area of ​​small and large fontanelles of the flat bones of the skull.
3. Dolichocephaly (long-headed) - an elongated skull
4. Pigeon (cock) breast
5. Rachitic rosary
6. Garrison's furrow - expansion of the lower part of the chest and its depression.
7. Bony epiphysis - the expanded end of the tubular bone
8. Rachitic pelvis
9. Curvature of the limbs

Residual effects of rickets

These are the remaining deformities of the skeleton and teeth, short stature, fermentopathy, underdevelopment of the muscular frame, deficiency of psychomotor development. And if psychosomatics can be improved, then malformations of the skeleton, posture disorders, and defects in the dentoalveolar rows remain for life.

Diagnosis of rickets

Diagnostic measures for rickets today are difficult and confusing. If previously a qualitative test for the content of calcium in the urine (Sulkovich's test) was considered reliable, it has now been rejected. Only the level of calcium in plasma can be considered reliable. Therefore, it is now customary to study the following blood parameters:

• the content of calcium, phosphorus, magnesium, alkaline phosphatase and creatinine in serum,
• levels of vitamin D metabolites.

An X-ray of the lower leg and forearm is also prescribed, on which a decrease in bone density is determined, the fuzziness of the boundaries of the zones of calcification of cartilage tissue, deformation of the metaphyses and expansion of growth zones.

There are 3 degrees of rickets in children

• With rickets 1 (mild), 1-2 bone manifestations are noted (from the side of the head, chest, limbs), there is muscle hypotension, but psychomotor development is not disturbed.
• At grade 2 (moderate course), bone deformities are more severe (legs, spine, sternum are deformed), lesions of the nervous system and internal organs are pronounced. There are deviations in the motor and mental components of the child's development.
• At grade 3 (severe), the bone deformities are multiple and persistent, the child lags behind in development, his hematopoiesis, digestion, cardiovascular and respiratory systems, and the central nervous system suffer.

How to treat rickets in babies

• General therapeutic and preventive measures for rickets in infants

Therapeutic measures begin with the normalization of the lifestyle and nutrition of the child. It is important that the child walked at least 4 hours a day, was in a ventilated and normally lit room. In spring and summer, it is important that the child receives a sufficient amount of sunlight. If possible, the child should be taken out for a walk as undressed as possible.

The best food for a child under one year old is breast milk with an optimal calcium-phosphorus balance. If it is impossible to establish breastfeeding, resort to adapted mixtures. It is important to introduce complementary foods in a timely manner. For a child suffering from rickets or threatened by its development, a single-component vegetable puree (zucchini, broccoli) is preferable as the first complementary food. It is important to monitor the balance of fats, since vitamin D is fat-soluble, and timely introduce vegetable and butter into the diet (see).

Important daily bathing in salt or coniferous baths. It calms the nervous system and strengthens the immune system.

• Medicines are used to treat and prevent rickets

Aquadetrim - Today, preference is given to aqueous solutions of vitamin D3 (cholecalciferol), for example, Aquadetrim. The drug is well absorbed and does not accumulate, being excreted by the kidneys. This allows you to use it without the risk of overdose for prevention and treatment. Prophylactic doses are given from the age of 4 weeks and range from 2 to 4 drops (depending on the region of residence, weight and condition of the child). Therapeutic dosages are selected by the doctor and increased gradually. On average, from 6 to 10 drops for 4-6 weeks, followed by care for preventive dosages. Prevention of rickets in infants is carried out throughout the autumn-winter period. For children in the northern regions, prevention is also carried out in the summer with insufficient insolation.

Devisol, Vigantol, Videin - Oil solutions of vitamin D3 (Vigantol, Videin). Of the imported drugs, Finnish Devisol is used. It does not cause allergies, therefore it is preferable for children with diathesis on Aquadetrim. But at the same time, the oil solution is not suitable for children with dysbacteriosis and absorption problems (see,). It is also quite problematic to titrate therapeutic dosages (the prophylactic dose of devisol is 5 drops).

An oil solution of vitamin D2 (Ergocalciferol) is used for prophylaxis, but taking oil solutions has a number of disadvantages, so it is prescribed less frequently.

Frequently asked Questions

How to determine rickets in infants?

An infant with rickets does not sleep well, shudders at loud noises, wakes up from the usual noises, and sweats a lot. He wipes the back of his head and spoils his appetite.

How big are the risks of vitamin D overdose?

For a child under the age of one year, when using an aqueous solution of vitamin D3 in the amount of 2 drops, an overdose does not threaten.

Does sunlight or quartz solve the problem of rickets?

Only in cases where the child is breastfed, tans from birth, walks every day and receives ultraviolet irradiation every day for at least half of the skin.

If the adapted milk formula contains vitamin D, can I not give drugs?

The milk mixture does not cover even the preventive need for the vitamin. Mothers of premature babies, those who were born with a weight of 4 kg or more, as well as frequently ill children, should be especially vigilant. For them, it is possible to start prophylaxis with drugs from 2 weeks of age.

Is it true that breastfed babies are more prone to rickets?

Nothing like this. In breast milk, the optimal ratio of calcium and phosphorus, moreover, during breastfeeding, their content and ratio ensures their better absorption.

Is it true that feeding with goat's milk protects against rickets?

A very dangerous misconception. Although this milk contains fats that promote the absorption of vitamin D, but they are three times more than normal, which can lead to damage to the pancreas. If milk is diluted three times so that it approaches breast milk in fat content, then its nutritional value in terms of protein is lost. In addition, children under one year old should not be given cow or goat milk.

Should a child older than a year be transferred to fish oil?

Children's endocrinologists have proven that fish oil has a negative effect on the pancreas and is less effective in preventing rickets than pharmacy vitamin D preparations.

- a disease of a fast-growing organism, characterized by a violation of mineral metabolism and bone formation. Rickets is manifested by multiple changes in the musculoskeletal system (softening of the flat bones of the skull, flattening of the occiput, deformity of the chest, curvature of the tubular bones and spine, muscular hypotension, etc.), nervous system, and internal organs. The diagnosis is established on the basis of the detection of laboratory and radiological markers of rickets. Specific therapy for rickets involves the appointment of vitamin D in combination with therapeutic baths, massage, gymnastics, UVI.

General information

Rickets is a polyetiological metabolic disease, which is based on an imbalance between the child's body's need for minerals (phosphorus, calcium, etc.) and their transportation and metabolism. Since rickets mainly affects children aged 2 months to 3 years, in pediatrics it is often called the "disease of the growing organism." In older children and adults, the terms osteomalacia and osteoporosis are used to refer to this condition.

In Russia, the prevalence of rickets (including its mild forms) is 54-66% among term infants and 80% among premature infants. Most children in 3-4 months have 2-3 mild signs of rickets, in connection with which some pediatricians suggest considering this condition as paraphysiological, borderline (similar to diathesis - anomalies of the constitution), which is independently eliminated as the body grows older.

Pathogenesis of rickets

The determining role in the development of rickets belongs to exogenous or endogenous vitamin D deficiency: insufficient formation of cholecalciferol in the skin, insufficient intake of vitamin D from food and impaired metabolism, which leads to a disorder of phosphorus-calcium metabolism in the liver, kidneys, and intestines. In addition, other metabolic disorders contribute to the development of rickets - a disorder of protein and microelement metabolism (magnesium, iron, zinc, copper, cobalt, etc.), activation of lipid peroxidation, multivitamin deficiency (deficiency of vitamins A, B1, B5, B6, C , E), etc.

The main physiological functions of vitamin D (more precisely, its active metabolites 25-hydroxycholecalciferol and 1,25-dihydroxycholecalciferol) in the body are: increased absorption of calcium (Ca) and phosphorus (P) salts in the intestine; obstruction of the excretion of Ca and P in the urine by increasing their reabsorption in the tubules of the kidneys; bone mineralization; stimulation of the formation of red blood cells, etc. With hypovitaminosis D and rickets, all of the above processes slow down, which leads to hypophosphatemia and hypocalcemia (low levels of P and Ca in the blood).

Due to hypocalcemia, secondary hyperparathyroidism develops according to the feedback principle. An increase in the production of parathyroid hormone causes the release of Ca from the bones and the maintenance of a sufficiently high level in the blood.

A change in the acid-base balance towards acidosis prevents the deposition of P and Ca compounds in the bones, which is accompanied by a violation of the calcification of growing bones, their softening and a tendency to deformation. Instead of a full-fledged bone tissue, osteoid non-calcified tissue is formed in the growth zones, which grows in the form of thickenings, tubercles, etc.

In addition to mineral metabolism, with rickets, other types of metabolism (carbohydrate, protein, fat) are also disturbed, disorders of the function of the nervous system and internal organs develop.

Causes of rickets

The development of rickets is largely associated not with exogenous vitamin D deficiency, but with its insufficient endogenous synthesis. It is known that more than 90% of vitamin D is formed in the skin due to insolation (UVR) and only 10% comes from outside with food. Only 10-minute local exposure of the face or hands can provide the synthesis of the level of vitamin D necessary for the body. Therefore, rickets is more common in children born in autumn and winter, when solar activity is extremely low. In addition, rickets is most common among children living in regions with a cold climate, insufficient natural insolation, frequent fogs and clouds, and unfavorable environmental conditions (smog).

Meanwhile, hypovitaminosis D is the leading, but not the only cause of rickets. Deficiency of calcium salts, phosphates and other osteotropic micro- and macroelements, vitamins in young children can be caused by multiple rachitogenic factors. Since the most enhanced intake of Ca and P to the fetus is observed in the last months of pregnancy, premature babies are more prone to developing rickets.

The increased physiological need for minerals in conditions of intensive growth predisposes to the occurrence of rickets. A deficiency of vitamins and minerals in a child's body may be the result of an improper diet of a pregnant or lactating woman, or the baby itself. Impaired absorption and transport of Ca and P contributes to the immaturity of enzyme systems or pathology of the gastrointestinal tract, liver, kidneys, thyroid and parathyroid glands (gastritis, dysbacteriosis, malabsorption syndrome, intestinal infections, hepatitis, biliary atresia, CRF, etc.).

The risk group for the development of rickets includes children with an unfavorable perinatal history. Adverse factors on the part of the mother are gestosis of pregnant women; hypodynamia during pregnancy; operational, stimulated or rapid childbirth; mother's age is younger than 18 and older than 36; extragenital pathology.

On the part of the child, a large weight (more than 4 kg) at birth, excessive weight gain or malnutrition can play a certain role in the development of rickets; early transfer to artificial or mixed feeding; restriction of the child's motor mode (too tight swaddling, lack of baby massage and gymnastics, the need for prolonged immobilization in case of hip dysplasia), taking certain medications (phenobarbital, glucocorticoids, heparin, etc.). The role of gender and hereditary factors has been proven: for example, boys, children with swarthy skin, II (A) blood group are more predisposed to the development of rickets; Rickets is less common among children with I (0) blood group.

Rickets classification

Etiological classification involves the allocation of the following forms of rickets and rickets-like diseases:

1. Vitamin D-deficientrickets(calcipenic, phosphoropenic variant)
2. Vitamin D dependent(pseudo-deficient) rickets with a genetic defect in the synthesis of 1,25-dihydroxycholecalciferol in the kidneys (type 1) and with genetic resistance of target organ receptors to 1,25-dihydroxycholecalciferol (type 2).
3. Vitamin D-resistant rickets(congenital hypophosphatemic rickets, Debre de Toni-Fanconi disease, hypophosphatasia, renal tubular acidosis).
4. Secondary rickets with diseases of the gastrointestinal tract, kidneys, metabolism or drug-induced.

The clinical course of rickets can be acute, subacute and recurrent; severity - mild (I), moderate (II) and severe (III). In the development of the disease, periods are distinguished: initial, peak of the disease, convalescence, residual effects.

Symptoms of rickets

The initial period of rickets falls on the 2-3rd month of life, and in premature babies in the middle - the end of the 1st month of life. Early signs of rickets are changes in the nervous system: tearfulness, fearfulness, anxiety, hyperexcitability, superficial, disturbing sleep, frequent shuddering in a dream. The child has increased sweating, especially in the scalp and neck. Sticky, sour-smelling sweat irritates the skin, causing persistent diaper rash. Rubbing the head against the pillow leads to the formation of foci of baldness on the back of the head. On the part of the musculoskeletal system, the appearance of muscular hypotension (instead of physiological muscle hypertonicity), compliance of the cranial sutures and the edges of the fontanel, thickenings on the ribs ("rachitic beads") is characteristic. The duration of the initial period of rickets is 1-3 months.

During the height of rickets, which usually falls on the 5-6th month of life, progression of the process of osteomalacia is noted. The consequence of the acute course of rickets can be softening of the cranial bones (craniotabes) and unilateral flattening of the occiput; deformity of the chest with depression ("cobbler's chest") or bulging of the sternum (keeled chest); the formation of kyphosis ("rachitic hump"), possibly lordosis, scoliosis; O-shaped curvature of tubular bones, flat feet; formation of a flat rachitic narrow pelvis. In addition to bone deformities, rickets is accompanied by an increase in the liver and spleen, severe anemia, muscle hypotension ("frog" belly), looseness of the joints.

In the subacute course of rickets, there is hypertrophy of the frontal and parietal tubercles, thickening of the interphalangeal joints of the fingers (“strings of pearls”) and wrists (“bracelets”), costal-cartilaginous joints (“rachitic beads”).

Changes in the internal organs in rickets are caused by acidosis, hypophosphatemia, microcirculation disorders and may include shortness of breath, tachycardia, loss of appetite, unstable stools (diarrhea and constipation), pseudoascites.

During the period of convalescence, sleep normalizes, sweating decreases, static functions, laboratory and radiological data improve. The period of residual effects of rickets (2-3 years) is characterized by residual deformation of the skeleton, muscle hypotension.

In many children, rickets is mild and not diagnosed in childhood. Children suffering from rickets often suffer from SARS, pneumonia, bronchitis, urinary tract infections, atopic dermatitis. There is a close relationship between rickets and spasmophilia (children's tetany). In the future, in children who have had rickets, there is often a violation of the timing and sequence of teething, malocclusion, enamel hypoplasia.

Diagnosis of rickets

The diagnosis of rickets is established on the basis of clinical signs, confirmed by laboratory and radiological data. To clarify the degree of violation of mineral metabolism, a biochemical study of blood and urine is carried out. The most important laboratory signs that allow you to think about rickets are hypocalcemia and hypophosphatemia; increased activity of alkaline phosphatase; decreased levels of citric acid, calcidiol and calcitriol. At research of KOS of a blood acidosis comes to light. Changes in urine tests are characterized by hyperaminoaciduria, hyperphosphaturia, hypocalciuria. Sulkovich's test for rickets is negative.

When radiography of tubular bones, changes characteristic of rickets are revealed: goblet expansion of the metaphyses, blurring of the boundaries between the metaphysis and epiphysis, thinning of the cortical layer of the diaphyses, indistinct visualization of the ossification nuclei, osteoporosis. Therapeutic mud can also be used to assess the state of bone tissue.

Forecast and prevention

The initial stages of rickets respond well to treatment; after adequate therapy, long-term effects do not develop. Severe forms of rickets can cause pronounced skeletal deformities, slowing down the physical and neuropsychic development of the child. Observation of children who have had rickets is carried out quarterly, for at least 3 years. Rickets is not a contraindication for prophylactic vaccination of children: vaccination is possible as early as 2-3 weeks after the start of specific therapy.

Prevention of rickets is divided into antenatal and postnatal. Prenatal prophylaxis includes the intake of special micronutrient complexes by a pregnant woman, sufficient exposure to fresh air, good nutrition. After childbirth, it is necessary to continue taking vitamins and minerals, breastfeeding, adhere to a clear daily routine, and conduct preventive massage for the child. During daily walks, the child's face should be left open for access to the skin of the sun's rays. Specific prevention of rickets in breastfed newborns is carried out in the autumn-winter-spring period with the help of vitamin D and UV radiation.

There are diseases that have long been considered “pre-revolutionary” and obsolete, but, as medical practice shows, they are not so rare and may sometimes not depend at all on the standard of living of the family, nursing and nutrition. These include in infants.

And now let's dwell on this in more detail.

What is rickets?

Internal diseases and genetic abnormalities

The situation is more complicated with children who have internal organs from birth:

• intestines,
• liver,
• kidneys.

Malabsorption in the intestines, obstruction (obstruction) of the biliary tract, genetic diseases that prevent the absorption of vitamin D - all this ultimately leads to the appearance of the first signs in infants, which is very difficult to treat.

Other factors

Prematurity and artificial feeding are two more important factors that directly affect the metabolic processes in the body and the absorption of nutrients from food.

The fact is that in premature babies, the need for vitamin D is significantly higher than in those born on time, so very often the food does not cover the vitamin deficiency: it only grows and worsens if the signs are not noticed in time and the nutrition system is not changed.

Artificial children suffer due to the fact that in cow's, goat's milk, artificial mixtures, the proportion of calcium and phosphorus, the most important building blocks for bone tissue, is disturbed.

It is important for mothers whose children do not receive breast milk to know that ideal mixtures and animal milk do not exist, therefore the nutrition of an artificial child must be built in such a way that the deficiency of vitamin D, calcium and phosphorus is constantly covered with complementary foods.

Rickets classification

The classification of rickets that exists in domestic pediatrics is associated with the effectiveness of vitamin D therapy. There are such types of the disease:

• Classic D-deficient is the most common;
• Secondary;
• Vitamin D-dependent;
• Vitamin D-resistant.

In turn, the classic is subdivided according to changes in the concentration of calcium and phosphorus in the blood, therefore, there are calcium-penic, phosphopenic forms of it, which indicate a significant deficiency of these important elements. Sometimes the classic proceeds with normal levels of calcium and phosphorus.

With caution, they are also prescribed to children receiving adapted milk formulas, which already contain vitamin D.

Rickets is a disease characterized by a violation of phosphorus-calcium metabolism. Usually this diagnosis is determined in children at an early age against the background of an insufficient amount of vitamin D in the body - calciferol. Chronic deficiency of this microelement leads to disruption of the supply of phosphorus and calcium to bone and cartilage tissue. As a result of this, irreversible changes occur in the formation and mineralization of bones, which causes rickets in children.

Most people consider this diagnosis a relic of years, so rickets is often called not a medical, but a social problem, since it is associated with a violation of the conditions for caring for a child. Undoubtedly, the modern standard of living of the population and the improvement of the general socio-economic situation in the country should help to make this disease a thing of the past.

But despite this, rickets still poses a threat to the health of children in the first years of life.

Rickets is a disease that affects the musculoskeletal system. Most clearly, the signs of pathology are manifested in infants and young children - a few months after birth and up to 5 years. Rarely, a similar situation develops in an adult, but in this case we are talking about osteomalacia - a pathological softening of the bones.

Changes in bone tissue against the background of rickets are caused by a chronic lack of phosphorus and calcium.

Usually, these trace elements are found in sufficient quantities in food, but in order for them to be fully absorbed by the body, vitamin D or calciferol is needed - a substance that helps phosphorus and calcium penetrate into bone and muscle tissue, into nerve fibers, pre-preparing them.

Vitamin D enters the body of children from food and special pharmacy supplements. Also, calciferol is independently formed in the skin of a child under the influence of direct ultraviolet rays from products of cholesterol derivatives (which is why any restrictions on baby food are prohibited).

The main causes of rickets are:

• malnutrition;
• insufficient exposure to open sunlight;
• disorders of vitamin D and cholesterol metabolism.

Also, experts identify a whole list of predisposing factors contributing to the development of rickets:

• the weight of the child is more than 4 kg at birth;
• refusal to breastfeed;
• the use of non-adapted mixtures for artificial feeding;
• difficult childbirth;
• restriction of motor activity of the child;
• rare walks;
• disruption of the digestive tract;
• frequent infectious and viral diseases;
• treatment with anticonvulsants;
• rapid growth and weight gain in a child requiring an increased amount of calcium in the body.

Usually, children born prematurely as a result of the disease are affected. They may develop symptoms of rickets as early as the second week after birth. This is due to the general weakness of their body and the unpreparedness of the digestive system to normally accept and assimilate food against the background of physiological immaturity.

The exception is the congenital form of rickets, the causes of which are the unsatisfactory condition of the placenta and the meager diet of the mother during pregnancy.

In rare cases, doctors are faced with rickets, independent of the presence of vitamin D in the body. In this disease, both calciferol, and phosphorus, and calcium are in the child's body within the normal range, but due to the existing pathologies in the liver and kidneys, as well as when taking certain medications (corticosteroids, barbiturates, etc.), calcium and phosphorus are not can be converted into an accessible form for full assimilation by the body.

Symptoms and Diagnosis

The first signs of rickets in children appear imperceptibly and most parents do not pay due attention to them, attributing everything to the whims and behavior of the child.

So, we list the main symptoms of the disease:

• problems with falling asleep, violation of the biological rhythm of sleep and wakefulness;
• sudden fearfulness of the child, unexplained anxious behavior;
• sluggish inhibited state, lack of interest in the surrounding reality;
• severe irritability, constant whims for no apparent reason;
• excessive sweating, especially during feeding, while the sweat has an unpleasant sour smell;
• irritation and itching of the skin;
• lack of hair in the occipital region due to the fact that the child rubs against the pillow during sleep;
• constant ammonia smell from the genitals, diaper rash and irritation on the genitals due to contact with urine;
• convulsive syndrome, especially during sleep;
• persistent digestive problems - diarrhea or constipation.

These signs of rickets usually develop a few months after the birth of a child. The onset of the disease usually occurs in the cold season - late autumn or winter-spring period.

The first symptoms of rickets affect the behavior of the child to a greater extent: he becomes extremely capricious and demanding, nervousness is associated with increased sweating, itching and skin irritation, characteristic baldness of the back of the head.

If you leave these symptoms without due attention, then by six months the child will already have a complete picture of the disease.

Following the first symptoms of the disease, a delay in physical development appears: the baby begins to raise and hold his head later, sit down and walk, he later has milk teeth, and the fontanel remains open longer than the due date.

Both the pediatrician and parents should definitely pay attention to all this and conduct a biochemical blood test in a timely manner: changes in the analysis will indicate a low concentration of phosphorus and an increased activity of phosphatase.

Signs of rickets that appear in a later period are already an independent irreversible pathology. The danger lies in serious developmental disorders, which later becomes the cause of disability.

Children's rickets affects cartilage and bone tissue, the immune system and internal organs. Children suffering from rickets from the first months of life are more likely to develop infectious and viral diseases.

The following symptoms indicate the complications of rickets:

• pathological enlargement of the spleen and liver;
• chronic anemia;
• abnormal joint mobility;
• hypotension of muscles, for example, the abdomen - it becomes flat and shapeless when the child lies on his back;
• unnatural curvature of the legs with the letters O or X (appears from the moment the child begins to walk);
• retraction or protrusion of the chest;
• rachiocampsis;
• rachitic growths on the ribs, visible to the naked eye;
• softening of the bones of the skull;
• bone growths along the superciliary arches, parietal and frontal protrusions;
• a noticeable increase in head volume;
• thickening of the ankles and wrists - rachitic "bracelets".

If treatment is delayed, the consequences can be catastrophic. In the future, a hump forms in the child against the background of a curvature of the spine, specific bone thickenings appear on it. Anatomically underdeveloped pelvis and pathological formation of cartilage and bone tissue lead to the development of hip dysplasia.

Also, the list of complications can be supplemented with flat feet, asymmetry of the skull and disability of the child. Residual symptoms of rickets remain with a person throughout his subsequent life. We are talking about a stable deformation of the skeleton.

The diagnosis is made on the basis of examination and laboratory and instrumental research methods. If rickets is suspected, the pediatrician sends a small patient for consultations to a pediatric surgeon and orthopedist, who know how to identify rickets at an early stage.

Specialists may prescribe the following additional studies:

• biochemical analyzes of urine and blood to determine the amount of phosphorus, calcium and calciferol;
• computed tomography and X-ray examination, which allows to examine the lesions of cartilage and bone tissue in the body.

Based on the diagnostic examination, the doctor selects the appropriate treatment or prescribes preventive measures.

Treatment

The primary task in the treatment of rickets is the biochemical normalization of the amount of missing trace elements in the body. A huge role in this case is played by specific drugs with vitamin D.

They are available in the form of tablets and drops and are used depending on the age of the child. With a therapeutic and prophylactic purpose, the following drugs are prescribed: Aquadetrim, Vigantol, Devisol and many others. The drug and dosage of the drug should be selected by the doctor according to an individual scheme.

Improving the child's condition against the background of conservative treatment occurs quickly, this can be seen from radiographic and biochemical changes. After the start of taking the drug with calciferol, within one week, the concentration of phosphorus increases significantly, the activity of alkaline phosphatase decreases, and the level of calcium in the blood temporarily decreases.

Positive changes also appear on the radiograph: the ossification nuclei become more visible, the bone tissues become stronger, and new epiphyseal lines are found.

The second point in the treatment of rickets is physiotherapy.

With its help, it is possible to accelerate the development of the child and the assimilation of trace elements by his body. Children suffering from rickets should move more, develop muscles and joints. Physiotherapy can be carried out as soon as the child is 6 months old.

Usually, the treatment complex includes massage, balneotherapy, electrophoresis using phosphorus and calcium ions, ultraviolet baths and therapeutic exercises.

Surgical treatment is necessary if the disease has passed into a severe stage.. In this case, vitamin therapy and massage become ineffective, since serious changes have occurred in the child's musculoskeletal system.

Bone deformities can only be corrected by surgery. It will help to give the bones and joints a natural physiological position. The recovery period after surgical treatment largely depends on the nutrition of the child, the presence in his body of the necessary trace elements and vitamins.

In most cases, rickets is not life threatening. But if you do not engage in the prevention and treatment of this disease, then its symptoms can subside over time, and the consequences will remain for the rest of your life.

Many children who have been ill at an early age with a mild form of rickets and have not received appropriate treatment, with age begin to suffer from caries, curvature of the legs, and even lag behind in physical and mental development.

Pathological changes affecting the bone and cartilage tissue cause flat feet, scoliosis and pelvic deformity.

At school age, such children are often diagnosed with myopia and anemia, and infectious and colds often occur. As adults, they suffer from osteoporosis and brittle bones.

Fortunately, today medicine can cope with this disease: the neglected form of rickets in modern children is becoming an exception.

At the same time, the task of parents remains paramount: not to miss the unpleasant symptoms of the disease, carefully monitor the development and condition of their child in order to maintain his health for many years.

Useful video about the signs of rickets in children

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Rickets

A disease of young children, in which, due to vitamin D deficiency, calcium-phosphorus metabolism, the processes of bone formation and mineralization, as well as the function of the nervous system and internal organs are disturbed.

"Classic" rickets remains a very common disease. It affects infants during a period of rapid growth: between the ages of 2 months and 2 years.

The occurrence of rickets in infants is associated with insufficient intake of vitamin D in his body.

It can enter the baby's body in two ways: firstly, with food, being absorbed in the intestines; secondly, being synthesized in the skin under the action of solar (ultraviolet) rays. In the future, under the influence of enzymes, it is activated in the cells of the liver and kidneys, after which it begins to fully fulfill its functions (first of all, it contributes to the deposition of calcium in the bones).

Due to the fact that an intensive intake of calcium and phosphorus from mother to fetus occurs only in the last months of pregnancy, a child of less than 30 weeks of prenatal period already at birth has a lower bone content of minerals. This is also facilitated by poor nutrition of a pregnant woman.

The immaturity of the enzyme systems of the liver, kidneys, skin, as well as their diseases, provoke the development of rickets, so it occurs especially often in premature babies.

For the normal process of ossification, it is important that there is a sufficient content of protein, calcium and phosphorus in the diet with their correct ratio, as well as trace elements of magnesium and zinc, vitamins of groups B and A.

Insufficient motor activity of the child also leads to rickets, since the blood supply to the bones increases significantly with muscle activity.

Signs of rickets in the initial period

The disease is clearly manifested at the age of 3-6 months, sometimes already at 1.5-2 months. In the initial period of rickets, there are changes in the activity of the nervous and muscular systems. The child becomes irritable, restless, shudders at loud sounds, the appearance of bright light, sleeps uneasily. He has increased sweating, especially of the head.

The kid rubs his head against the pillow, and soon baldness of the back of the head sets in. You may notice an ammonia smell from wet diapers. After 2-3 weeks from the onset of the disease in infants, softness of the bone edges in the region of the large fontanel, along the sutures of the skull, is found. Muscle tone is reduced. Such signs are characteristic of rickets of the 1st degree. This period lasts from 1.5 weeks to 1 month.

Height period.

At this stage of the disease, symptoms of a disorder of the nervous and muscular systems increase. The child has increased sweating, weakness, hypotension of muscles and ligamentous apparatus.

This period of rickets is especially characterized by the rapid progression of bone changes: softening of the flat bones of the skull, flattening of the occiput, and asymmetric shape of the head. The growth of immature bone tissue at the ossification points of the flat bones of the skull leads to the formation of frontal and occipital tubercles. Because of this, the baby's head takes on a square or buttock-like shape, the skull becomes asymmetrical.

The baby may experience deformities of the facial part of the skull - a saddle nose, an "Olympic" forehead. The teeth of a child with rickets are cut later, inconsistently, in the future they are easily affected by caries. Due to the looseness of the ligaments, the baby can easily reach his head with his feet and even suck his toes. Low muscle tone leads to an increase in the abdomen (flattened, "frog" abdomen), provoking the formation of a hernia.

The chest with rickets is also often deformed. On the ribs, at the junction of the cartilaginous and bone parts, "beads" are formed; "chicken breast" (protrusion of the sternum in the form of a keel) may form; rachitic curvature of the spine in the form of a hump or lateral. At the level of attachment of the diaphragm outside, on the chest, the child has a deep retraction - "Harrison's furrow", and the lower ribs, due to the large belly, are turned forward in the form of hat fields. Depending on the timing of the appearance of rickets in a baby, a variety of curvature of the lower extremities is possible, of which the most common are O-shaped legs.

If rickets continues when the child has learned to step over in the crib, he may end up with X-shaped legs. As a rule, rickets is accompanied by flat feet.

In a child with severe rickets (3 degrees), in addition to the bone, other systems and organs are also affected. There are deafness of heart sounds, palpitations, systolic murmur, prolonged inflammation of the lungs develops, the liver and spleen increase. The baby's lag in psychomotor development becomes noticeable, the development of conditioned reflexes slows down, and the acquired skills weaken or completely disappear.

The course of rickets depends on the child, the nature of feeding, the season of the year and weather sensitivity, the characteristics of the regimen, education, and how well the disease is prevented. The onset and exacerbation of the disease are observed, as a rule, in late autumn, winter and early spring. In the summer, the process subsides and recovery occurs.

If therapeutic measures are not taken or they are insufficient, the infant develops a subacute course of rickets with moderate changes in the neuromuscular and skeletal systems. But even mild forms of rickets, with subtle external manifestations, reduce the resistance of the child's body, which creates the preconditions for the emergence of other diseases (respiratory infections, anemia), often with complications.

If the child gets into unfavorable conditions, and the treatment of rickets is stopped, with an incorrect regimen and excessive carbohydrate nutrition, especially in winter, the disease takes a relapsing course.

In premature babies, rickets is characterized by an early onset (2-3 weeks of life), a predominance of bone changes, and mild neurological symptoms. Bone changes in a baby are manifested by softening of the temporal regions, flattening of the nape, and an increase in the size of a large fontanel. Such signs of rickets as sweating, baldness of the temporal areas, anxiety, poorly expressed in the early stages of the disease by the end of the 2-3rd month of the baby's life.

Complex therapy of rickets in a child includes:

Calcium and phosphorus preparations;

Properly organized dietary and hygienic regimes;

Vitamin D or UVR;

Vitamins C, A, group B;

A citrate mixture containing citric acid, ATP;

Massage and gymnastics.

Specific prophylaxis and therapy

To prevent rickets in a baby at risk, prevention consists in taking vitamin D from 2-4 weeks of age. A daily dose of 400-500 IU of vitamin D per day is clearly insufficient to prevent rickets. According to domestic researchers, among children who received this dose for prophylactic purposes, rickets occurs in 50-80.6%.

A child with a small large fontanel or its early closure has only relative contraindications to D-vitaminization, and the danger of hypervitaminosis D in this case should be considered exaggerated. Such a baby is usually carried out delayed specific prevention of rickets, starting from 3-4 months of life.

Non-specific methods of prevention and treatment

Therapy without the use of vitamin D includes the organization of the correct sanitary and hygienic regime - with sufficient exposure of the child to fresh air, walks in any season of the year, good sleep, provided that the baby is protected from excessive external stimuli (noise, light). During wakefulness, the infant's mental and motor activity should be stimulated.

A child suffering from rickets needs good nutrition and additional doses of vitamins C and group B (B1, B2, B6). A breastfed baby needs calcium supplements. A citrate mixture is widely used, which is given to a child 1 teaspoon 3-4 times a day for 1-1.5 months.

The diet depends on the age of the child. The best option in the first year of life is natural feeding.

If the child is on mixed or artificial feeding and receives adapted mixtures, the presence of vitamin D in them should be taken into account (doses per 1 liter of the mixture are indicated on the packages).

It is advisable to treat a child older than six months with the help of various therapeutic baths: coniferous, salt and herbal decoctions. Coniferous baths are useful for an excitable baby, salt baths are best taken by a child with severe pastosity ("looseness") of the subcutaneous fat base, as well as a sluggish and inactive one, and baths with decoctions of medicinal herbs are recommended for a baby with concomitant exudative diathesis.

Feeding a baby creates additional vitamin D requirements for the mother. The daily requirement of a nursing woman is 1200 mg of calcium and 800 IU of vitamin D.

Special control over the observance of preventive measures is taken in relation to children at risk. These include premature, immature babies and those with low body weight; infants suffering from diathesis, food allergies, chronic intestinal diseases; children receiving anticonvulsant therapy. All babies with impaired intestinal absorption syndrome, with reduced motor activity, need the prevention of rickets.

The latter group includes infants who are being treated for hip dysplasia or certain neurological conditions.

Nutrition for a child with rickets

The diet of an infant suffering from rickets should solve the following problems:

Provide an optimal level of protein and the best conditions for the absorption of calcium and phosphorus;

Be rich in vitamins C, B1, B2, A;

Correspond to the condition of the gastrointestinal tract and the age of the baby;

Exclude unilateral predominance of products, be diverse.

If a child who is on mixed or artificial feeding has signs of rickets, it is necessary to use adapted mixtures with a higher content of vitamin D (up to 400 IU per 1 liter of reconstituted product).

The ratio of calcium to phosphorus in these mixtures should be 1.5:1 or 2:1.

It is advisable to introduce fermented milk products into the diet of such an infant, which have a beneficial effect on the absorption of nutrients, including calcium, by the body. Juices and fruit purees can be introduced into the diet of a baby with manifestations of rickets from 1.5-2 months of age. At the same time, attention should be paid to the content of vitamin C, calcium and phosphorus salts in them. These substances are richer in black currant, rosehip, lemon, orange, dogwood, cherry, sweet cherry and persimmon.

Complementary foods in the form of vegetable puree are introduced ahead of schedule using the widest range of vegetables. It is desirable to enrich the puree with well-chopped garden greens, which are a rich source of vitamin C, calcium and phosphorus salts. It is necessary to give the child an egg yolk in a timely manner, rich in fat-soluble vitamins, calcium salts, phosphorus and trace elements. It also contains vitamin D. At an earlier date, cottage cheese and meat are introduced into the baby's diet as sources of animal protein and calcium.