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We are accustomed to considering rickets as a unique disease of its kind, caused by a significant lack of vitamin D in the body and, accordingly, a deficiency of its active derivatives. In fact, this is a group of diseases provoked by a violation of mineral metabolism, primarily by a low content of calcium and phosphorus in the blood plasma. And the reason for this condition is a deficiency of many substances coming from outside or synthesized in the body.

As a result of salt imbalance, the formation of bone tissue is disrupted and the functions of many internal organs are affected. Pathology occurs both in childhood and in adulthood. But today we will talk about the classic form of rickets, which mainly affects children: almost half of children under the age of three experience single or multiple symptoms of the disease. Rare forms of the disease are hereditary in nature, are much less common, and doctors unanimously included them in the list of rickets-like.

Classic rickets develops during a period of active human growth, which means that the most striking symptoms occur in infants and young children. Let's figure out why this happens, why the disease is dangerous, and how you can protect your little one from it.

The basis of bone tissue is calcium phosphate. It is formed as a result of complex physical and chemical processes. A regulates salt metabolism not only by vitamin D, but also by A, group B, C, E, thyroid and parathyroid hormones, the concentration of the minerals themselves, the rate of their elimination from the body, and the quantity and quality of transport proteins also play a role.

As a result of a breakdown at at least one of the stages, either a sufficient amount of calcium phosphate does not enter the bone or it is washed out into the blood to maintain internal homeostasis (for the functioning of more important structures). Bone tissue becomes loose and soft or, conversely, processes of perverted synthesis begin in it. The main symptoms of the disease are associated with this.

Causes of rickets and risk factors

Knowing the causes of the disease, you can determine the risk factors for the development of classic rickets.

Risk factors

During pregnancy:

• toxicosis, but more often;
• pathology of the formation and functioning of the placenta;
• renal or hepatic pathology, hypovitaminosis D in a pregnant woman;
• physical inactivity and insufficient insolation during the gravity period;
• short break between pregnancies;
• mother's age is too young.

After birth

• genetic predisposition;
• —prematurity—and low weight, accompanied by immaturity of enzymatic systems for processing vitamins;
• intensive growth in weight and size of the bone skeleton;
• debilitating chronic diseases, pathology of the respiratory tract leading to hypoxia;
• unbalanced diet;
• birth during the season of insufficient insolation (autumn, winter);
• drug deficiency, hypocalcemia and hypophosphatemia.

What are the signs of rickets in children

After you become familiar with the clinical signs of the disease, you will realize that many of them are familiar to you from your own children, nephews, neighbor kids... The disease is polysymptomatic, but a certain sequence of the appearance and progression of symptoms can still be traced.

The first signs of classic rickets appear in infants 2-3 months of age, and are characterized by changes in the function of the autonomic nervous system:

• anxiety;
• poor sleep;
• flinching;
• sweating of the skin on the back of the head (the child subconsciously wipes himself on the pillow, as a result of which this area becomes bald);
• sweating of the body skin, complicated by prickly heat, itching and increased skin sensitivity.

At the same time, signs of changes in bone tissue appear, with the rapidly growing parts of the skeleton being affected first:

• during the first 3 months of life, signs of damage to the skull become noticeable;
• from 3 months to six months, the chest and torso are involved in the process;
• as soon as the load appears on the legs, they also suffer (from 6 months).

The nature of bone damage depends on the course of the pathology:

• in the acute period, the phenomena of softening and, accordingly, deformation predominate;
• in subacute – excessive synthesis of non-calcified bone tissue.

And now directly about the signs of classic rickets in children under 1 year of age.

Head

During the period of intensive growth of the skull bones, the baby mainly lies down, and as the bone tissue softens, flattening forms in the corresponding places, leading to deformation and asymmetry of the head. The fontanelles heal slowly (up to 2 years), their edges soften and become pliable. In the subacute period, the frontal and parietal tubercles grow, giving the head a square shape.

At an older age, the normal parameters of the head are restored, but the appearance of teeth is observed later. Subsequently, such children are much more prone to caries than healthy ones.

Rib cage

In acute cases, as a result of increased softness, flattening is formed in those places where the load falls. Usually this:

• lateral depressions of the ribs with protrusion of the sternum in the form of a keel and curvature of the clavicles (with frequent lying on the side);
• transverse depression along the anterior surface of the chest at the level of the attachment of the diaphragm, curvature of the spine backwards or to the sides (when sitting).

The growth of bone tissue is manifested by the so-called rosary - thickenings in the shape of large beads at the junction of the bone and cartilaginous parts of the ribs (along the lateral edges of the sternum).

Limbs

As a result of softening of the pelvic bones, the latter becomes flattened. When bone tissue is damaged, children who begin to stand or walk develop curvature of the legs with a bend in the knee area outward (in the shape of the letter O) or inward (letter X).

With excess synthesis, thickenings appear in different places:

• in the place of the wrist joint - “rachitic bracelets”;
• in the area of ​​the finger phalanges - “strings of pearls”;
• above the ankle joint.

All these signs of rickets in infants are clearly visible in the photos presented in any relevant literature.

Muscles and joints

Their defeat is also characteristic of pathology. The muscles become flabby and sluggish, and cannot keep the joints toned. Joint looseness appears, and the child can unnaturally straighten his limbs, bend his fingers, throw his leg behind his head (like a gutta-percha boy). Flabbiness of the abdominal press is manifested by a large “frog” belly and divergence of the rectus muscles.

Other signs

A severe course, in addition to damage to the central nervous system and bone skeleton, is characterized by enlargement of the liver, lymph nodes and spleen, and disruption of the cardiovascular and digestive systems. Thoracic deformation and weakness of the diaphragmatic muscle gradually lead to impaired ventilation of the lungs, which increases the risk of developing.

Why is rickets dangerous?

A mild course with mild changes in the nervous and skeletal systems does not pose a danger, except that babies later begin to roll over, sit, crawl, stand and walk, they erupt teeth later than usual and have a weakened immune system. But after moderate and severe forms, persistent residual effects can be observed for up to 2-3 years, in the worst case – lasting a lifetime:

• developmental delay;
• bone deformities;
• flat feet;
• myopia;
• liver enlargement;
• signs of immunodeficiency;
• caries;
• enlarged spleen.

What tests are needed to make a diagnosis?

1. An experienced pediatrician only needs to look at the child to make a diagnosis. But to treat pathology and monitor therapy, it is necessary to accurately know the level of minerals in plasma and urine, as well as the degree of damage to the skeletal system. For this purpose, a biochemical blood test and x-ray examination are performed. Blood is taken on an empty stomach, preferably in the morning. No specific preparation is required for x-rays.
2. If a moderate or severe degree is suspected, a comprehensive examination is carried out, including ultrasound, to clarify the condition of the internal organs and identify the possible cause of the disease.

How to treat rickets in a child

For pathologies of mild to moderate severity, it is not necessary to be treated in a hospital. The entire course can be completed on an outpatient basis. Severe damage requires constant medical supervision; it is treated under the control of calcium and phosphorus levels in the blood and urine, and, depending on the tests, the dosage of drugs is adjusted.

Regardless of the severity of the symptoms of rickets in children, doctors prescribe drug (specific) therapy and nonspecific treatment (daily routine and diet).

Nutrition and daily routine

1. Diet therapy consists of correcting the nutrition of the nursing mother, and after the introduction of complementary foods, of the child.
2. To stimulate the synthesis of vitamin D in the skin, frequent and long walks are recommended (just not in direct sunlight). They also contribute to better aeration of the lungs. And when the child learns to walk, even with outside help, he is prescribed an enhanced motor regimen.
3. Not earlier than 21 days from the start of drug therapy, full body massage and physical therapy are prescribed (passive for the smallest, i.e., active for older children).
4. They also resort to prescribing medicinal baths (pine baths for easily excitable children and salt baths for passive ones).
5. Thermal procedures in the form of paraffin baths or warming with sand are prescribed to the affected joints.

Drug treatment of rickets

Of course, these are vitamins, primarily D, and calcium supplements (in the acute stage), magnesium, and potassium. If there are signs of damage to muscle tissue and parenchyma of internal organs, symptomatic therapy (ATP, antianemic drugs, etc.) is indicated. The course of treatment lasts 1-1.5 months. The dosage of drugs for specific therapy depends on the severity of the pathology.

After completing the course, the child is given a citrate mixture for a month, although it can be prescribed in small doses simultaneously with vitamin D. The last stage of treatment is ultraviolet radiation, carried out in courses with a break of 1.5-2 months. If signs of relapse of the disease appear, a second course is possible no earlier than 3 months after the end of the first (not in summer).

Is it possible to get vaccinated for rickets?

Mild pathology is not a contraindication to vaccination. Moreover, one of its complications may be immunodeficiency. And when vaccines are administered, the child’s immunity begins to activate.

In cases of moderate and severe severity, vaccinations are delayed until the baby has fully recovered (3 months after the disappearance of active signs of the disease).

How to protect your child from rickets

Prevention of rickets in children begins in the prenatal period. Pregnant women are recommended to have a balanced diet, physical activity, and fresh air. If there is a hereditary predisposition, vitamin D is prescribed after the 7th obstetric month or ultraviolet radiation in the autumn-winter season (up to 20 sessions).

After birth, it is recommended to breastfeed the baby or with adapted formulas, walk in the fresh air, do massage and do gymnastics. In the risk group, specific prevention is carried out by prescribing vitamin D from one month of age. Older children are prescribed a diet that must contain lactic acid products, butter and vegetable oils, egg yolk, liver, and sea fish in their dishes. These foods are rich in calcium and vitamin D.

Be a support and support for your child from the first days of life. Affectionate communication, maternal and paternal care will give him confidence. He will be less capricious, willingly eat and walk in the fresh air with his loved ones.

Video: drug prevention of rickets

From the short video you will learn the name of a specific drug, the time of its prophylactic use and contraindications for use.

In our country, children rarely develop severe forms of rickets. But we can see signs of a mild form all the time. That is why you were offered a brief description of the pathology. If you know even more about it, share your knowledge in the comments.

In addition to classic bone changes with a predominance of osteomalacia, symptoms of increased excitability (hand tremors, sleep disturbance, unmotivated anxiety) are noted. Children also have a severe disorder of the autonomic nervous system (excessive sweating, tachycardia, white dermographism).

A biochemical blood test against the background of a significant decrease in calcium levels reveals a high concentration of parathyroid hormone and a reduced concentration of calcitonin. Characterized by increased excretion of calcium in the urine.

Phosphopenic rickets

General lethargy, lethargy, severe muscle hypotonia and weakness of the ligamentous apparatus, “frog belly”, and signs of hyperplasia of osteoid tissue are noted.

Characterized by severe hypophosphatemia, high levels of parathyroid hormone and calcitonin in the blood serum, and hyperphosphaturia in the urine.

Rickets without pronounced changes in the concentrations of calcium and phosphorus in the blood

Patients with this form of rickets, as a rule, do not have clear clinical changes in the nervous and muscular systems. The disease is characterized by a subacute course with signs of hyperplasia of osteoid tissue (parietal and frontal tubercles).

Symptoms of rickets: damage to the nervous system

Functional disorders of the nervous system are the initial symptoms of rickets. They manifest themselves in the form of anxiety, tearfulness, sleep disturbances, shuddering during sleep, and severe sweating. The head sweats especially heavily in the back of the head. Sticky sweat irritates the skin, causing itching. The child rubs his head on the pillow, and, as a result, baldness of the back of the head appears - a characteristic sign of incipient rickets.

An important symptom of rickets from the nervous system is hyperesthesia. Often, when trying to be picked up, the child cries and worries.

With severe rickets, changes in the central nervous system are noted: general motor retardation, children become sedentary, slow, and the development of conditioned reflexes becomes difficult.

Symptoms of rickets: damage to the skeletal system

The entire skeleton is typically affected, but clinical manifestations are more pronounced in those bones that grow most rapidly at a given age. Thus, when rickets occurs in the first 3 months of life, changes appear in the bones of the skull. As the disease develops from 3 to 6 months, changes are found in the bones of the chest. When children over 6 months of age develop rickets, the bones of the limbs and pelvis are affected. There are 3 options for changing bones:

• osteomalacia;
• osteoid hyperplasia;
• osteoporosis.

Symptoms of osteomalacia

• Damage to the bones of the skull. Softening of the edges of the large fontanel and sutures, craniotabes [areas of softening of the body of the skull bone (the occipital bone is most often affected)] are noted. The sensation obtained by pressing on these areas can be compared to pressing on parchment or a felt hat. The softness of the bones of the skull leads to its deformations: flattening of the back of the head or the side surface, depending on how the child lies more.
• Damage to the bones of the chest. As a result of softening of the ribs, Harrison's groove is formed (at the site of attachment of the diaphragm, retraction of the ribs is noted, the lower aperture of the chest is deployed), and curvature of the clavicles. The chest is compressed from the sides, the sternum protrudes forward or sinks.
• Damage to the bones of the limbs. Their curvature is noted. The child's legs take on an O- or X-shape.

Manifestations of osteoid hyperplasia

• Bone damage skulls There is an increase in the frontal, parietal, occipital mounds.
• Damage to the bones of the chest. Formation of rachitic “rosary beads” on the ribs (ribs V-VIII) at the site of transition of bone tissue into cartilaginous tissue.
• Damage to the bones of the limbs. The appearance of “bracelets” on the wrist, “strings of pearls” on the fingers.

Changes in the skeletal system with rickets

Muscular system

Important symptoms of rickets are weakness of the ligamentous apparatus and muscle hypotonia. Weakness of the ligamentous apparatus leads to “looseness” of the joints, which allows the patient to make movements of greater volume (for example, lying on his back, a child easily pulls his foot towards his face and even throws it behind his head). The patient's posture is typical - he sits with his legs crossed and supports his torso with his hands. Hypotonia of the muscles of the anterior abdominal wall is manifested by a flattened abdomen with divergence of the rectus muscles (“frog belly”). Static functions are disrupted: children later begin to hold their head up, sit, stand, walk, and they develop a “rachitic hump.”

Dysfunction of other organs and systems

• In some children, at the height of rickets, hypochromic anemia is detected.
• Enlargement of the liver and spleen (hepatolienal syndrome) is often noted.
• Changes in the chest and hypotonia of the muscles lead to respiratory disorders with rickets of II-III degree. Children develop shortness of breath, cyanosis, and pulmonary ventilation is impaired. Areas of atelectasis in the lungs may occur, predisposing to the development of pneumonia.
• Violations of chest excursion and insufficient contraction of the diaphragm lead to hemodynamic disturbances, which are manifested by tachycardia, muffled heart sounds, and functional systolic murmur.
• In some cases, pathology is noted with aspects of the digestive and urinary system.

Periods of rickets

The period of the disease is determined by the clinical picture, the severity of osteomalacia and biochemical changes.

Symptoms of rickets in the initial period

More often it occurs in the 2-3rd month of life and lasts from 2-3 weeks to 2-3 months.

Disturbances of the autonomic nervous system are characteristic, and only at the end of this period changes in the skeletal system appear in the form of pliability of the edges of the large fontanel and sagittal suture.

From the muscular system, hypotension and constipation are noted.

A biochemical blood test reveals a slight decrease in phosphorus levels, while calcium levels remain normal. An increase in alkaline phosphatase activity is characteristic.

Symptoms of rickets during the peak period (“blooming” rickets)

Characterized by progressive lesions of the nervous and skeletal systems. Bone changes come to the fore. All 3 types of changes are noted (osteomalacia, osteoid hyperplasia, osteogenesis disorder), but their severity depends on the severity and course of the disease.

In addition, the peak period is characterized by:

• distinct muscle hypotonia;
• weakness of the ligamentous apparatus;
• enlarged liver and spleen;
• hypochromic anemia;
• functional disorders of other organs and systems.

The number of systems involved and the severity of their changes depend on the severity of the process.

A biochemical blood test reveals significantly reduced levels of calcium and phosphorus and increased alkaline phosphatase activity.

Symptoms of rickets during the period of convalescence

Reverse development of rickets symptoms is noted. The first to disappear are the symptoms of damage to the nervous system, then the bones become denser, teeth appear, changes in the muscular system disappear (static and motor functions are normalized), the size of the liver and spleen decreases, and dysfunction of the internal organs is restored.

Phosphorus levels increase to normal values; calcium concentration may remain reduced, alkaline phosphatase activity increased.

Symptoms of rickets in the period of residual effects

It is observed in children older than 2-3 years. During this period, only the consequences of rickets persist in the form of bone deformations, which indicate that the child suffered a severe form of the disease (I or III degree). No deviations in laboratory parameters of mineral metabolism were noted.

Thanks to the subsequent processes of bone tissue remodeling, which occur most actively after 3 years, deformations of the tubular bones disappear over time. Deformations of flat bones decrease, but remain. In children who have suffered from rickets, enlargement of the parietal and frontal tubercles, flattening of the occiput, malocclusion, deformation of the chest and pelvic bones remain.

The severity of rickets

I degree (mild)

A small number of mild signs of rickets from the nervous and skeletal systems with the involvement of the 1st-2nd sections of the skeleton in the process. Sometimes mild muscle hypotonia is observed.

After grade I rickets, no residual effects are noted.

II degree (moderate)

III degree (severe)

Currently almost never found. It manifests itself as significant changes in the central nervous system: sleep disturbance, appetite, lethargy, retardation in the development of speech and motor skills. Changes in the skeletal system have the character of multiple, clearly expressed deformations (softening of the bones of the base of the skull, retraction of the bridge of the nose, “Olympic” forehead, gross deformation of the chest, limbs, pelvic bones). Bone fractures without displacement or with angular displacement are possible. There are pronounced changes in the muscular system (impaired static functions). The liver and spleen are significantly enlarged, there are clear functional disorders of the cardiovascular system and respiratory organs. Gastrointestinal tract, severe anemia.

The nature of the course of rickets

Acute course

Rapid increase in symptoms, predominance of osteomalacia processes over osteoid hyperplasia processes. It is observed more often in the first half of life, especially in premature, overweight, and frequently ill children.

– a disease of a rapidly growing organism, characterized by impaired 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, deformation of the chest, curvature of the tubular bones and spine, muscle hypotonia, etc.), nervous system, and internal organs. The diagnosis is established based on the identification of laboratory and radiological markers of rickets. Specific therapy for rickets involves the administration of vitamin D in combination with therapeutic baths, massage, gymnastics, and ultraviolet radiation.

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 a “disease of the growing body.” 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 full-term young children and 80% among premature infants. Most children at 3-4 months have 2-3 mildly expressed signs of rickets, and therefore some pediatricians suggest considering this condition as paraphysiological, borderline (similar to diathesis - constitutional anomalies), which is eliminated on its own as the body matures.

Pathogenesis of rickets

The decisive role in the development of rickets belongs to exo- or endogenous vitamin D deficiency: insufficient formation of cholecalciferol in the skin, insufficient intake of vitamin D from food and disruption of its 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 - metabolic disorders of protein and microelements (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: enhancing the absorption of calcium salts (Ca) and phosphorus (P) in the intestine; preventing the excretion of Ca and P in the urine by increasing their reabsorption in the kidney tubules; mineralization of bone tissue; stimulation of red blood cell formation, 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 maintains its sufficiently high level in the blood.

A change in acid-base balance towards acidosis prevents the deposition of P and Ca compounds in the bones, which is accompanied by impaired calcification of growing bones, their softening and tendency to deformation. Instead of 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, rickets also disrupts other types of metabolism (carbohydrate, protein, fat), and disorders of the nervous system and internal organs develop.

Causes of rickets

The development of rickets is largely associated not with exogenous deficiency of vitamin D, 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. Just 10 minutes of local irradiation of the face or hands can provide the synthesis of the level of vitamin D required by 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 levels of natural insolation, frequent fog and cloudiness, 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 ricketogenic factors. Since the most increased supply of Ca and P to the fetus is observed in the last months of pregnancy, premature babies are more prone to developing rickets.

The occurrence of rickets is predisposed by an increased physiological need for minerals under conditions of intensive growth. A deficiency of vitamins and minerals in a child’s body can be a consequence of an improper diet by a pregnant or lactating woman, or by the baby herself. Impaired absorption and transport of Ca and P is facilitated by 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, chronic renal failure, etc.).

The risk group for the development of rickets includes children with an unfavorable perinatal history. Unfavorable factors on the part of the mother are gestosis in pregnant women; physical inactivity during pregnancy; operative, induced or rapid labor; mother's age is younger than 18 and older than 36 years; extragenital pathology.

On the part of the child, a certain role in the development of rickets can be played by a large weight (more than 4 kg) at birth, excessive weight gain or malnutrition; 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 long-term immobilization for hip dysplasia), taking certain medications (phenobarbital, glucocorticoids, heparin, etc.). The role of gender and hereditary factors has been proven: thus, boys, children with dark skin, blood group II (A) are more predisposed to the development of rickets; Rickets is less common among children with blood group I (0).

Classification of rickets

The etiological classification involves the identification of the following forms of rickets and rickets-like diseases:

1. Vitamin D deficiencyrickets(calciumpenic, phosphopenic variant)
2. Vitamin D dependent(pseudo-deficiency) 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 for diseases of the gastrointestinal tract, kidneys, metabolism or induced by drugs.

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

Symptoms of rickets

The initial period of rickets occurs in the 2-3rd month of life, and in premature infants 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, shallow, anxious sleep, frequent startles in sleep. The child's sweating increases, especially in the scalp and back of the head. Sticky, sour-smelling sweat irritates the skin, causing persistent diaper rash. Rubbing your head against a pillow leads to the formation of bald spots on the back of your head. The musculoskeletal system is characterized by the appearance of muscle hypotonia (instead of physiological muscle hypertonicity), compliance of the cranial sutures and edges of the fontanel, thickenings on the ribs (“rachitic rosary”). The duration of the initial period of rickets is 1–3 months.

During the height of rickets, which usually occurs in the 5-6th month of life, the process of osteomalacia progresses. The consequence of the acute course of rickets can be softening of the cranial bones (craniotabes) and unilateral flattening of the back of the head; deformation 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 enlarged liver and spleen, severe anemia, muscle hypotonia (“frog” belly), and loose joints.

In the subacute course of rickets, hypertrophy of the frontal and parietal tubercles, thickening of the interphalangeal joints of the fingers (“strings of pearls”) and wrists (“bracelets”), and costochondral joints (“rachitic rosaries”) occur.

Changes in the internal organs during rickets are caused by acidosis, hypophosphatemia, microcirculation disorders and may include shortness of breath, tachycardia, loss of appetite, unstable stool (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 skeletal deformation and muscle hypotonia.

In many children, rickets occurs in a mild form and is not diagnosed in childhood. Children suffering from rickets often suffer from acute respiratory viral infections, pneumonia, bronchitis, urinary tract infections, and atopic dermatitis. There is a close connection between rickets and spasmophilia (infantile tetany). Subsequently, children who have suffered from rickets often experience a violation of the timing and sequence of teething, malocclusion, and 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 disturbance of mineral metabolism, a biochemical study of blood and urine is performed. The most important laboratory signs that allow us to think about rickets are hypocalcemia and hypophosphatemia; increased alkaline phosphatase activity; decreased levels of citric acid, calcidiol and calcitriol. A blood CBS test reveals acidosis. Changes in urine tests are characterized by hyperaminoaciduria, hyperphosphaturia, hypocalciuria. Sulkovich's test for rickets is negative.

X-rays of tubular bones reveal changes characteristic of rickets: goblet-shaped expansion of the metaphyses, unclear boundaries between the metaphysis and the epiphysis, thinning of the cortical layer of the diaphysis, unclear visualization of the ossification nuclei, osteoporosis. Therapeutic mud can also be used to assess the condition of bone tissue.

Prognosis and prevention

The initial stages of rickets respond well to treatment; after adequate therapy, long-term consequences do not develop. Severe forms of rickets can cause severe skeletal deformations and slow down the physical and neuropsychic development of the child. Monitoring of children who have suffered rickets is carried out quarterly for at least 3 years. Rickets is not a contraindication for preventive vaccination of children: vaccinations are possible within 2-3 weeks after the start of specific therapy.

Prevention of rickets is divided into antenatal and postnatal. Prenatal prevention includes taking the pregnant woman special micronutrient complexes, sufficient exposure to fresh air, and nutritious nutrition. After childbirth, it is necessary to continue taking vitamins and minerals, breastfeeding, adhere to a clear daily routine, and give the child preventive massage. During daily walks, the child's face should be left exposed to 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 ultraviolet radiation.

Parents often have many questions about rickets. Let's look at the most common of them.

Question 1. What is rickets?

This is a disease of children in the first three years of life, which is associated with a discrepancy between the baby’s needs for calcium and phosphorus and their intake. This imbalance leads to disruption of bone formation, functioning of the nervous system and internal organs. One of the causes of rickets is a deficiency of vitamin D. This vitamin, acting on tissues, maintains the normal metabolism of phosphorus and calcium.

Vitamin D can be taken into the body through food and formed in the skin in the sun under the influence of ultraviolet rays. Its sources are meat, fish, egg yolk, butter, human and cow's milk. In addition, a child can receive this vitamin in the form of a medicine, which is prescribed to prevent rickets.

Most often, rickets develops in the first year of life. At the age of 2–3 years, as a rule, its consequences are already observed, manifested in the form of bone deformations.

Question 2. How to recognize rickets in a child?

The initial signs of rickets usually appear in the first months of a child’s life. The baby becomes irritable, restless, flinches at loud sounds or bright light. His sleep becomes restless. Excessive sweating occurs, which leads to the development of prickly heat, which is difficult to treat.

Miliaria is characterized by a rash in the form of small red spots, and sometimes groups of small blisters filled with clear liquid. They can be found in the area of ​​natural folds, in the cervical, axillary and groin areas, and on the back. Sweating of the head causes itching, the child begins to rub his head on the pillow, which leads to baldness at the back of the head.

Muscle tone is reduced, the child is lethargic, inactive, and the muscles become flabby. The baby periodically experiences stool retention for up to 2–3 days.

Question 3. Why does rickets occur?

The following factors contribute to the development of rickets:

• High growth rates of children at an early age and an increased need for mineral components (calcium, phosphorus), which make up bone tissue. Therefore, the risk group includes premature babies, babies with a birth weight of more than 4 kg, with large weight gain in the first 3 months of life.
• Deficiency of calcium and phosphorus in food due to malnutrition. A lack of vitamins A, C, group B (especially B1, B2, B6), folic acid, as well as zinc, copper, iron, magnesium, manganese, etc. also plays a major role in the development of rickets. This especially applies to children on artificial and mixed feeding with non-adapted milk formulas.
• Impaired absorption of calcium and phosphorus in the intestine, increased excretion in the urine or impaired entry into the bones. This may be due to the immaturity of transport systems that facilitate the transfer of calcium to bone tissue, or to diseases of the intestines, liver and kidneys, when the absorption of substances from food is impaired.
• Vitamin D deficiency, which regulates the metabolism of calcium and phosphorus in the body, is only one of the factors in the development of rickets. A lack of this vitamin can occur when there is insufficient intake of it from food or when the child is rarely exposed to the sun. It is known that vitamin D is formed in the skin under the influence of ultraviolet rays.

Question 4. Does rickets really develop only due to a lack of vitamin D?

Manifestations of the disease cannot be considered a consequence of insufficient intake into the body alone. Deficiency of this vitamin is only one of the factors contributing to the development of rickets. The development of bone manifestations of rickets in young children is primarily due to rapid growth rates, high rates of skeletal changes and a lack of phosphorus and calcium in the growing body when their intake into the body is disrupted.

Question 5. Are parents right in believing that if a baby spends a lot of time in the open sun, he will not have rickets?

As already mentioned, deficiency is only one of the factors in the development of rickets. Therefore, its sufficient formation in the body under the influence of sunlight does not mean that the baby cannot get sick. If a child spends a lot of time in the sun, but there are other risk factors (prematurity, severe liver or kidney disease, improper feeding, etc.), the baby may also develop rickets.

In addition, it is necessary to avoid direct sunlight on the baby's skin - this is dangerous due to burns. For the formation of vitamin D in the skin, diffused light is enough, so it is more beneficial for children to sunbathe in the shade of trees. Walking with a child in the open sun from 10 a.m. to 5 p.m. in summer is not recommended.

The duration of the first sunbath in the warm season should be no more than 5–6 minutes, then the time spent in the sun gradually increases to 8–10 minutes 2–3 times during a morning walk. If the weather permits, in the summer the child should take daily sunbathing. Using children's sunscreen cosmetics makes your baby's exposure to the sun safe and beneficial.

Question 6. Is it true that if a child is breastfed, he is not at risk of rickets?

Breast milk is known to contain all the essential nutrients in the right quantity and in a balanced state. Calcium in it is in an optimal ratio with phosphorus and is well absorbed by the child’s body. But milk has all the beneficial properties only if the nursing mother is healthy and eats fully and correctly. Thus, breastfeeding does not guarantee that the baby will not develop rickets, especially if there are other risk factors (for example, prematurity, insufficient sun exposure, etc.). Therefore, all breastfed children are prescribed prophylactic vitamin D3, excluding the summer months.

Question 7. If a baby has lost the hair on the back of his head, does this necessarily mean that he has developed rickets?

Balding of the back of the head does not always indicate the development of rickets. After birth, the baby's vellus hair gradually changes. This process occurs most intensively at the age of 2–4 months. The hair follicles of the vellus hair are weakly fixed, so when they rub against the pillow, they fall out more intensely in the back of the head. Thus, baldness in this area may be a manifestation of physiological hair change.

Question 8. If a baby has a flat back of the head, is this already advanced rickets?

Flattening of the occiput is one of the initial manifestations of rickets in children in the first six months of life, when, due to softening of the bone tissue, the shape of the skull changes. With timely treatment, the baby recovers and the bones acquire the correct shape.

Question 9: Should the doctor do any tests to make a diagnosis?

In most cases, the diagnosis is established based on the collection of information about childbirth, the child’s nutrition, his growth and development, and changes that the doctor discovers when examining the baby.

The severity of the disease and the period of rickets can be clarified by a biochemical blood test, which evaluates the content of calcium, phosphorus and alkaline phosphatase activity (with rickets, the analysis shows a decrease in the content of calcium and phosphorus in the blood and an increase in the activity of alkaline phosphatase). An x-ray examination of the bones of the forearm is also prescribed (it is performed in rare cases, if it is necessary to determine the severity and period of the disease).

Question 10. What medications does a sick baby need?

Vitamin D preparations are used in the treatment of rickets. This name combines a whole group of substances, the main ones being vitamin D2 (ergocalciferol) and vitamin D3 (cholecalciferol).

To normalize the function of the parathyroid glands, which are involved in the regulation of calcium and phosphorus metabolism in the body, and to reduce the severity of symptoms from the nervous system, magnesium preparations are included in the complex treatment of rickets.

Question 11. Besides medications, what does a child suffering from rickets need?

Treatment of rickets should be comprehensive. In addition to the use of medications, the following measures are necessary:

It is necessary to properly organize the child’s daily routine, providing sufficient rest in accordance with his age; eliminate various irritants (bright light, noise, etc.). It is recommended to take him for walks in the fresh air more often during daylight hours. These activities normalize the functioning of the baby’s nervous system and activate metabolism.

Rational nutrition is an important factor in the treatment of rickets. Feeding your baby breast milk is extremely important. It is known that mother's milk contains all the necessary nutrients, including calcium and phosphorus in a balanced amount that is optimal for absorption. In case of forced transfer of a child to mixed or artificial feeding, it is recommended to use an adapted milk formula, which is as close in composition as possible to human milk and enriched with all necessary minerals and vitamins. Your pediatrician will help you choose the mixture. Babies suffering from rickets, both breastfed and bottle-fed, are introduced to complementary foods earlier than healthy children.

After 2 weeks from the start of treatment, physical therapy and. During different periods of the disease, massage courses differ from each other. During the height of rickets, a course of general strengthening and physical therapy is usually prescribed. The procedures can be performed by a children's massage therapist or mother - after preliminary training by a specialist. During the period of residual effects, the purpose of massage is to reduce and eliminate disorders of the musculoskeletal system. It is better to entrust this course to an experienced children's massage therapist.

After 1 month from the start of treatment, balneotherapy can be used. Easily excitable children are prescribed pine baths: 1 teaspoon of pine extract is diluted in 10 liters of water at a temperature of 36 °C. The duration of the first bath should not exceed 5 minutes, subsequent ones - 8-10 minutes. The course consists of 13–15 procedures. For lethargic, sedentary children, salt baths are recommended: 2 tablespoons of sea or table salt are dissolved in 10 liters of water at a temperature of 36 °C. The first procedure lasts no longer than 3 minutes, subsequent ones – 5 minutes each. The course is 8–10 baths. Balneotherapy is carried out 2–3 times a year.

Therapeutic exercise and massage strengthen the muscular and skeletal systems weakened by the disease, activate metabolic processes, and improve the supply of nutrients to tissues. Balneotherapy improves muscle tone and normalizes the functioning of the baby’s nervous system.

Question 12. Can rickets go away without treatment?

If a child has manifestations of rickets, it means that his body already has a deficiency of calcium and phosphorus, which do not enter the bone tissue. With further intensive growth of the baby in the first year of life, the need for these substances increases, and adequate supply to the bone tissue in the absence of treatment does not occur; accordingly, the growth and development of the skeleton continues to be impaired. Therefore, it is necessary to establish a sufficient supply of calcium, phosphorus and vitamin D to the body. If all factors leading to the disease are not eliminated and metabolism is not normalized with the help of medications, nutrition and daily routine, rickets will progress and the disease will become more severe .

It is important for parents to understand that rickets is a disease that can be avoided with proper prevention. But if a child is nevertheless diagnosed with such a diagnosis, there is no need to panic: treatment started in the early stages of the disease leads to a complete recovery of the baby.

If rickets is not treated...

The duration of the initial period of the disease, the manifestations of which we discussed above, usually ranges from 2-3 weeks to 2-3 months and depends on the child’s living conditions and factors contributing to the development of rickets. Under the influence of treatment and elimination of the causes predisposing to rickets, the disease can result in complete recovery.

If treatment is not carried out, the period of the height of the disease begins. More pronounced bone changes appear. One of the early signs of this period in children in the first six months of life is softening of the back of the parietal bones and occipital bone. As a result, the skull changes its shape, the back of the head flattens, and asymmetry of the head occurs. As a result of the restructuring of bone tissue, the frontal and parietal tubercles begin to protrude more clearly, and the entire skull takes on a square shape, sometimes the bridge of the nose sinks (a “saddle” nose) or the forehead protrudes strongly. Another symptom of bone damage is the appearance of “rosary beads” on the ribs (the so-called thickenings at the junction of the cartilaginous part of the rib into the bone).

Teeth in children with rickets erupt very late, randomly and with large intervals in time. Also characteristic is the late closure of the large fontanel, which normally occurs on average by 12 months.

In the second six months of life, as the load on the bones increases, when the baby tries to sit, curvature of the spine, deformation of the chest, pelvic bones and legs appear. Muscle tone decreases, and weakness of the ligamentous apparatus (joint laxity) is noted. Reduced tone of the abdominal muscles leads to the appearance of a characteristic “frog” belly (it increases in size, and when lying on the back, it spreads out in different directions and becomes spread out). The formation of inguinal and umbilical hernias is also possible (the organs of the abdominal cavity or underlying tissues from the cavities occupied by them emerge under the skin without violating its integrity). The child lags behind in motor development: he begins to hold his head up, roll over, sit, and walk later. Most children with rickets experience anemia (lack of hemoglobin, a protein that carries oxygen to the body's cells) and decreased immunity, which leads to frequent respiratory diseases (for example, ARVI).

After a period of height comes a period of recovery. The child’s well-being improves significantly, changes in the nervous system disappear, muscle tone is normalized. The level of calcium and phosphorus in the blood returns to normal. But bone deformities remain. Meanwhile, with timely treatment, the skeletal system develops normally.