slide 2
Rickets is a disease of young children caused by a lack of vitamin D, essential amino acids and minerals.
slide 3
A 4-year-old girl with vitamin D-dependent rickets (side view): saber-varus deformity of the lower extremities, deformity of the skull and chest, rickety bracelets are noted.
slide 4
Causes of rickets in children:
Inadequate intake of calcium and phosphorus with food due to improper feeding. Increased need for minerals in conditions of intensive growth (rickets is a disease of a growing organism). Violation of the transport of phosphorus and calcium in the gastrointestinal tract, kidneys, bones due to the immaturity of enzyme systems or the pathology of these organs. Unfavorable ecological situation (accumulation of lead, chromium, strontium salts in the body, deficiency of magnesium, iron). Endocrine disorders (impaired functions of the parathyroid and thyroid glands). Exo- or endogenous deficiency of vitamin D.
slide 5
X-ray of the upper limb of a 7-month-old child: thinning and fibrillation of the cortical layer of the bones of the forearm, fringed subchondral contour of the distal metaphyses.
slide 6
X-ray of the lower extremities of a child aged 1 year 4 months: typical rachitic deformity of the tibia
Slide 7
Pathogenesis
In general, the pathogenesis of rickets is very complex, characterized by a violation of not only mineral, but also other types of metabolism, which has a multifaceted effect on the functional state of various organs and systems and, first of all, contributes to the disruption of bone formation processes.
Slide 8
Slide 9
Clinic
The initial period is characterized by a violation of the nervous system, and only at the end of this period there are changes in the skeletal system - pain on palpation of the bones of the skull, compliance of the edges of the large fontanel. The initial period lasts from 2-3 weeks to 2-3 months.
Slide 10
slide 11
The peak period is characterized by a progressive course of the disease. In the first place are changes in the skeletal system (craniotabes, frontal and parietal tubercles, late and incorrect teething, "rosary" on the ribs, expansion of the lower aperture and its deformation, rachitic "bracelets" and curvature of the legs). There are signs of muscle hypotension, weakness of the ligamentous apparatus, a delay in the development of static and motor functions, anemia often develops, an increase in parenchymal organs. There are functional changes in the respiratory and cardiovascular systems.
slide 12
Rickets deformity of the shins Complication - saddle nose Frog belly Muscular hypotension
slide 13
The period of convalescence is the weakening and reverse development of symptoms. First of all, symptoms from the nervous system disappear, bones become denser, teeth appear, static and motor functions develop, the size of the liver and spleen decreases, and dysfunctions of internal organs are gradually eliminated. In the blood test - an increase in phosphorus, and calcium is reduced.
Slide 14
The period of residual effects develops at the age of 2-3 years as a result of rickets II - III degree - bone deformity, changes in the teeth, sometimes the liver and spleen are enlarged, anemia of varying severity.
slide 15
There are three degrees of severity I degree mild II degree moderate III degree severe
slide 16
I degree of severity is characterized by a change in the skeletal system at 2-3 months of life, compliance and soreness appear on palpation of the bones of the skull, the edges of the large fontanelle, thickening is outlined on the ribs against the background of changes in the autonomic nervous system
Slide 17
II degree of rickets is characterized by pronounced changes in the skeletal system. As a result of hyperplasia of the bone tissue, parietal and frontal tubercles, "rachitic rosary" are formed, the ribs become soft, pliable, the chest is deformed, flattened, the lower aperture expands
Slide 18
According to the line of attachment of the diaphragm, retraction of the ribs-Harrison's groove appears - one of the pathognomonic signs of rickets. Pronounced hypotonia of muscles and weakness of the ligamentous apparatus. A "frog belly" appears - a flattened belly.
Slide 19
Grade III severe rickets softens the bones of the skull, the skull presses on the cervical vertebrae, the bridge of the nose seems to be very sunken, an "Olympic forehead" appears, deformity of the sternum ("shoemaker's chest" or "chicken breast"), in the spine there is an arcuate curvature posteriorly with kyphosis.
Slide 20
According to the nature of the course, they are distinguished: acute, subacute and recurrent. Acute in the first months of life - pronounced changes in the nervous system, the predominance of bone softening processes (osteomalacia) and in the blood test, a decrease in phosphorus and an increase in alkaline phosphatase.
slide 21
Subacute course - the symptoms of osteoid hyperplasia prevail, a slower course of the process. . It is noted in children 9-12 months old, patients with malnutrition, in children who received an insufficient dose of vitamin D. Recurrent - a change in the period of improvement, a period of deterioration.
slide 22
Additional and laboratory research methods
The diagnosis of rickets is established on the basis of data from the examination of the child by a doctor in conjunction with the results of laboratory tests. Sulkovich's test is referred to laboratory research methods that allow to make or exclude the diagnosis of rickets. This is a urinalysis that measures the amount of calcium in the urine. In turn, the amount of calcium excreted in the urine may indicate a lack or excess of intake and synthesis of vitamin D in the body. + calcium excretion in the urine is increased (within the normal range) ++ indicates that the child is healthy +++ the maximum allowable dose of vitamin D ++++ overdose of vitamin D - requires its urgent cancellation
slide 23
X-ray - signs of osteoporosis, the contours of the bones are blurred, the ends of the bones are goblet, the edges of the metaphyses are fringed. In the biochemical analysis of blood - a decrease in the amount of phosphorus, and the amount of calcium is within the normal range.
slide 24
Forecast
with rickets depends on the severity, the timeliness of diagnosis and the adequacy of treatment. If rickets is detected in the initial stage and adequate treatment is carried out, taking into account the polyetiology of the disease, the consequences do not develop. In severe cases, rickets can lead to severe skeletal deformities, slowing down of neuropsychic and physical development, visual impairment, and also significantly aggravate the course of pneumonia or gastrointestinal diseases. However, severe consequences often develop in extreme situations (in conditions of war, famine, etc.). Under normal conditions, if such consequences of rickets are suspected, other causes of such changes should first be excluded.
View all slides
Rickets is a polyetiological disease of early age, which is a consequence of metabolic disorders, mainly phosphorus-calcium, accompanied by damage to many organs and systems, the development of skeletal deformity. The disease has been known since ancient times. The first medical description of this pathology was given by the English anatomist and orthopedist F. Glisson in 1656. The name of the disease comes from the Greek word "rachis", which means "spine" (spine), the curvature of which is one of the symptoms of the disease. Rickets is one of the most common diseases in young children. According to various researchers, rickets occurs in 20-60% of children. Reliable data are unknown, since mild forms of the disease, initial manifestations are often missed.
Etiology The causes of rickets are divided into endogenous and exogenous. Endogenous: 1. Inadequate intake of vitamin D, phosphates, calcium, magnesium, zinc and other trace elements, vitamins, amino acids. 2. Insufficient exposure of the child to fresh air and insufficient insolation, which leads to a violation of the formation of vitamin D from 7-dehydrocholesterol in the epidermis under the influence of ultraviolet rays. Exogenous factors: 1. Violation of the absorption of vitamin D in the intestine. 2. Violation of the processes of hydroxylation of inactive forms of vitamin D into active forms (D) in the liver and kidneys. 3. Violation of the absorption of phosphorus and calcium in the intestine, their increased excretion in the urine, impaired utilization by bone tissue. 4. Violation of the functional activity of receptors for vitamin D.
Factors contributing to the development of rickets in children. 1. Artificial feeding 2. Prematurity of children (polyvitaminosis, including hypovitaminosis D, increased need for vitamin D, immaturity of morphological and functional systems). 3. High growth rate of the skeleton, rapid remodeling of bone tissue. 4. Poor child care.
Eating large amounts of grain products with food Insufficient UV exposure Insufficient intake of vitamin D with food Lack of vitamin D Decreased reabsorption of P in the kidneys Hypophosphatemia Cleavage of P from the myelin of nerve trunks Muscle hypotension Decreased synthesis of CaSB Decreased absorption of Ca in the intestine Hypocalcemia Hyperproduction of PTH Inhibition of citrate synthetase activity Inhibition of citrate synthesis Acidosis Violation of protein and other types of metabolism Aminoaciduria Violation of collagen synthesis Violation of the formation and deposition of CaHPO in bones Stimulation of osteoclasts Inhibition of osteoblasts Demineralization of bones Disturbance of bone formation
Working classification of Lukyanova E.M. (1988) distinguish: 1) Classical vitamin D-deficient rickets. 2) Vitamin D-dependent rickets is associated with a genetic defect in the synthesis of 1,25(OH) D in the kidneys or with the resistance of target organs to it. 3) Vitamin D-resistant rickets (tubulopathy, hypophosphatasia). 4) Secondary rickets in liver diseases, malabsorption syndrome, etc.
Diagnosis of rickets 1. Clinical data. 2. Biochemical analysis of blood: decrease in the concentration of phosphorus; decrease in phosphorus concentration; increased activity of alkaline phosphatase; increased activity of alkaline phosphatase; calcium content - N or hypocalcemia; calcium content - N or hypocalcemia; decrease in the content of citric acid (hypocythremia). decrease in the content of citric acid (hypocythremia). 3. X-ray of the bones of the skeleton - osteoporosis.
Clinical manifestation of rickets (SO Dulitsky, 1947) I degree 1. The first symptoms of rickets are vegetative disorders: sleep disorders; sleep disorders; irritability; irritability; tearfulness; tearfulness; increased sweating: most of the face, scalp; increased sweating: most of the face, scalp; "sour" sweat rubbing the head against the pillow nape baldness; "sour" sweat rubbing the head against the pillow nape baldness; Red dermographism. Red dermographism. 2. Compliance of the bones - the edges of the large fontanelle of the small fontanelle of the swept suture, (minor osteoporosis).
Grade II More pronounced bone changes appear: 1. Head: craniotabes (softening of parts of the parietal bones, less often parts of the occipital bone); craniotabes (softening of areas of the parietal bones, less often areas of the occipital bone); deformation of the bones of the skull; deformation of the bones of the skull; frontal and parietal tubercles; frontal and parietal tubercles; violation of the ratio between the upper and lower jaws; violation of the ratio between the upper and lower jaws; late closure of the large fontanel, violation of teething (untimely, incorrect), defects in tooth enamel. late closure of the large fontanel, violation of teething (untimely, incorrect), defects in tooth enamel.
2. Thorax: deformation of the clavicles (increased curvature); clavicle deformity (increased curvature); "costal rosary" (hemispherical thickening at the point of transition of the cartilaginous part of the rib to the bone); "costal rosary" (hemispherical thickening at the point of transition of the cartilaginous part of the rib to the bone); expansion of the lower aperture and narrowing of the upper one, compression of the chest from the sides; expansion of the lower aperture and narrowing of the upper one, compression of the chest from the sides; Navicular depressions on the lateral surfaces of the chest; Navicular depressions on the lateral surfaces of the chest; Deformation of the sternum ("keeled", "leuco-shaped" chest). Deformation of the sternum ("keeled", "leuco-shaped" chest). 3. Spine: Kyphosis in the lower part of the thoracic vertebrae, kyphosis or lordosis in the lumbar region, scoliosis in the thoracic region, flat pelvis. Kyphosis in the lower part of the thoracic vertebrae, kyphosis or lordosis in the lumbar region, scoliosis in the thoracic region, flat pelvis.
III degree 1. Deformity of the bones of the skull, chest, spine + various changes in the tubular bones: a) upper limbs: curvature of the humerus and bones of the forearm; curvature of the humerus and bones of the forearm; Deformity in the joints: "bracelets" (thickening in the area of the wrist joints), "strings of pearls" (thickening in the area of the diaphysis of the phalanges of the fingers). Deformity in the joints: "bracelets" (thickening in the area of the wrist joints), "strings of pearls" (thickening in the area of the diaphysis of the phalanges of the fingers). b) lower extremities: curvature of the hips forward and outward; curvature of the hips forward and outward; various curvature of the lower extremities (O- or X-shaped deformities); various curvature of the lower extremities (O- or X-shaped deformities); deformities in the joints. deformities in the joints.
Initial period 1. Occur for 2, 3 months. life, in premature babies - at the end of the first month. In the first place are changes in the nervous system: anxiety, slight excitability, startling at a sharp sound, disturbed sleep, increased sweating, mild muscle hypotension. anxiety, slight excitability, startling at a sharp sound, disturbed sleep, increased sweating, mild muscle hypotension.
Peak period 1. Bone deformities of varying degrees. 2. Severe muscular hypotension: "frog" belly; "frog" belly; looseness of ligaments and joints; looseness of ligaments and joints; symptom of "penknife"; symptom of "penknife"; symptom of "muffled"; symptom of "muffled"; Harrison's furrow. Harrison's furrow. 3. Late formation of static and motor functions (children begin to sit, stand, walk later). 4. Muscular hypotension chest deformity pulmonary ventilation disorders increased respiratory morbidity.
Period of residual effects 1. Deformations of flat bones decrease, but there are enlarged parietal and frontal tubercles, flattening of the occiput, deformity of the chest, pelvic bones, malocclusion. 2. Deformations of tubular bones disappear with time. 3. "Rachitic flat feet" changes in the axis of the lower extremities - in some children.
Acute course The predominance of osteomalacia processes over osteoid tissue hyperplasia (“craniotabes”, softening of the fontanel edges and sutures) more often in children of the first half of life, in premature babies, in children from multiple pregnancies who do not receive prophylactic doses of vitamin D. The predominance of osteomalacia processes over osteoid tissue hyperplasia ("craniotabes", softening of the edges of the fontanelles and sutures) more often in children of the first half of life, in premature babies, in children from multiple pregnancies who do not receive prophylactic doses of vitamin D.
Subacute course The predominance of hyperplasia of osteoid tissue in the areas of bone growth ("rib beads", "bracelets", "bumps", etc.). The predominance of hyperplasia of the osteoid tissue in the areas of bone growth ("costal beads", "bracelets", "bumps", etc.). More common in the second half of the year, in children receiving an insufficient prophylactic dose of vitamin D. More common in the second half of the year, in children receiving an insufficient prophylactic dose of vitamin D.
Recurrent course Repeated exacerbation of the subsided rachitic process. Repeated exacerbation of the subsided rachitic process. An x-ray examination of the bones reveals strips of calcification in the metaphyseal zones of tubular bones. An x-ray examination of the bones reveals strips of calcification in the metaphyseal zones of tubular bones. This course is more typical for secondary or hereditary forms of rickets. This course is more typical for secondary or hereditary forms of rickets.
Treatment of rickets It is necessary to eliminate the causes that led to the development of the disease; pathological changes that have occurred in the body. Treatment is divided into non-specific and specific. Nonspecific treatment: rational nutrition; balanced diet; the correct mode of the child; the correct mode of the child; sufficient exposure to fresh air; sufficient exposure to fresh air; daily hygienic, periodically medicinal coniferous and with sea salt. daily hygienic, periodically medicinal coniferous and with sea salt.
Specific treatment Specific treatment depends on the period of the disease and its course. In the initial period of the disease with a subacute course in full-term children, a general UVR is prescribed every day or every other day, sessions. UVR starts with 1/8 biodose and is adjusted to 1.5 biodose. In the initial period of the disease with a subacute course in full-term children, a general UVR is prescribed every day or every other day, sessions. UVR starts with 1/8 biodose and is adjusted to 1.5 biodose. At the height of the disease, vitamin D is prescribed by IU per day for 3-4 weeks. Mostly use an aqueous solution of vitamin D (cholecalciferol), 1 drop contains 500 IU. During treatment with vitamin D, it is advisable to carry out the Sulkovich test once a week (determination of the level of calcium in the urine.) At the height of the disease, vitamin D is prescribed by IU per day for 3-4 weeks. Mostly use an aqueous solution of vitamin D (cholecalciferol), 1 drop contains 500 IU. During treatment with vitamin D, it is advisable to carry out the Sulkovich test once a week (determining the level of calcium in the urine.) After achieving a therapeutic effect, they switch to a prophylactic dose (IU per day), which the child is prescribed for 2 years.
Prevention Antenatal and postnatal prophylaxis is carried out. Antenatal prophylaxis 1. Non-specific measures: Rational nutrition of a pregnant woman, adequate lifestyle, sufficient exposure to fresh air. Rational nutrition of a pregnant woman, an adequate lifestyle, sufficient exposure to fresh air. Prevention in and Russo-bacterial and other diseases in a pregnant woman. Prevention in and Russo-bacterial and other diseases in a pregnant woman. Timely treatment of gestosis of pregnant women. Timely treatment of gestosis of pregnant women. Prevention of miscarriage. Prevention of miscarriage. 2. Specific prophylaxis: It is carried out in the last 2-3 months of pregnancy in the autumn-winter period of the year. Vitamin D is prescribed by IU every day or UVI, sessions every day or every other day (start with ¼ biodose and increase to 2.5-3 biodoses). It is carried out in the last 2-3 months of pregnancy in the autumn-winter period of the year. Vitamin D is prescribed by IU every day or UVI, sessions every day or every other day (start with ¼ biodose and increase to 2.5-3 biodoses).
Postnatal prophylaxis 1. Non-specific: Breastfeeding, timely introduction of supplements and complementary foods. Breastfeeding, timely introduction of supplements and complementary foods. Carrying out massage and gymnastics (30-40 minutes a day). Carrying out massage and gymnastics (30-40 minutes a day). Sufficient exposure to fresh air, air baths. Sufficient exposure to fresh air, air baths.
2. Specific prophylaxis: Starts from 3-4 weeks (for premature babies from the day of life). Every day, the child is given an IU of vitamin D for up to a year. In the summer months (2-3 months), vitamin D is not given due to intense insolation. For premature babies and children with increased skin pigmentation, the daily dose of vitamin D is increased to IU and given for 1.5-2 years, excluding the summer months. For premature babies and children with increased skin pigmentation, the daily dose of vitamin D is increased to IU and given for 1.5-2 years, excluding the summer months. If children are fed with adapted mixtures, vitamin D is not prescribed. If children are fed with adapted mixtures, vitamin D is not prescribed. For the prevention of hypervitaminosis D, a Sulkovich test is necessary once every 2-7 weeks. For the prevention of hypervitaminosis D, a Sulkovich test is necessary once every 2-7 weeks.
Literature 1. A handbook for students of the highest medical initial pledges of the IV level of accreditation / For red. prof. O.V.Tyazhkoy/ Seeing a friend. - Vinnitsa: New book, - from Pediatrics: A textbook for students of higher medical. Proc. Institutions III-IV levels of accreditation. - 2nd ed., Rev. and additional /V.G. Maidannik. - Kharkov: Folio, - Rickets (Manual for doctors) / Romanyuk F.P., Alferov V.P., Kolmo A.E., Chugunova O.V. - St. Petersburg, - 62 p.
Rickets
This is a state of the body in which phosphorus-calcium metabolism is disturbed and the functions of all organs and systems are disrupted.
The cause of the disease is hypovitaminosis D
Pathogenesis disease is associated with malabsorption of phosphorus and calcium in the small intestine, which is regulated by vitamin D.
A decrease in the level of calcium in the blood increases the release of parathyroid hormone and causes the excretion of calcium from the bones.
Hypophosphatemia causes damage to the nervous system - excitation processes predominate, which are replaced by inhibition reactions. In muscle tissue, energy metabolism is disturbed and tone decreases. Metabolic disorders lead to functional, and then to morphological changes in the internal organs - respiration and digestion.
Rickets classification.
There are active and inactive (period of residual effects) phases of the disease.
In the active phase, the following periods of the disease are distinguished:
1 period - initial manifestations:
There are signs of damage to the nervous system.
The first signs appear on the 2nd month of a child's life
(in preterm infants at the end of the 1st month of life).
The behavior of the child changes: there is anxiety, rapid excitability, startling at a loud sound, superficial sleep, anxious, there is increased sweating during anxiety, feeding, in a dream. Sweat has a sour smell, irritates the skin, causes itching, the child rubs his head against the pillow, baldness appears on the back of the head, prickly heat, persistent red dermographism.
On palpation of the bones of the skull, their compliance is determined, but there are no obvious changes in the skeleton.
Sulkovich's test is weakly positive.
Length of the initial period:
in acute rickets is 2 - 6 weeks,
with subacute - delayed up to 2 - 3 months.
2nd period - peak period:
this period falls on the 5th-6th month of the child's life, sharp sweating persists, weakness, fatigue appear, pronounced hypotension of muscles and joints. There are pronounced changes in the skeleton, especially in areas of bone growth. The back of the head flattens, then the chest is deformed - the lower aperture expands, retraction appears along the attachment of the diaphragm - Harrison's groove, "chicken breast or shoemaker's chest", the tubular bones of the legs are bent - O - or X - figuratively, a flat rachitic pelvis is formed. Changes in bone tissue are manifested by the formation of frontal and parietal tubercles, overhanging superciliary arches, costal rosaries, rickety bracelets and strings of pearls. Fontanelles close by 1.5-2 years, teeth erupt late, the psychomotor development of the child slows down sharply.
Joint laxity, muscle hypotension,
frog belly.
deployed
lower aperture
chest
rachitic
rosary on chest
cage
chicken breast
Shoemaker's Chest
rachitic hump
Child lagging behind
neuropsychic development
On the radiograph of tubular bones
at the height of the disease are detected:
significant blur,
fuzzy growth zones,
bone osteoporosis.
3 period -
convalescence period -
this period is characterized by an improvement in the state and well-being, neurological disorders disappear, the functions of internal organs, psychomotor development are normalized, but muscle hypotension and skeletal deformity persist for a long time.
4 period - the period of residual phenomena - characterized by normalization of muscle tone, reduction and disappearance of looseness of the joints and ligaments, but gross bone changes remain.
According to the severity of the symptoms of rickets, there are:
Rickets 1st degree – mild - characterized by neuromuscular
manifestations and minor bone manifestations.
Rickets 2 degrees - moderate - in addition to neuromuscular
changes, there are distinct deformities of the skull, thoracic
cells, limbs, functional disorders
internal organs.
Rickets 3 degrees - severe - manifested by pronounced
musculoskeletal changes, joint laxity,
a sharp slowdown in the psychomotor development of the child,
dysfunction of internal organs.
According to the course of the disease, there are:
1- acute course - observed in children with unilateral,
carbohydrate nutrition, rapidly growing and adding to
the mass of children who did not receive prophylactic doses of vitamin D.
The rapid development of all symptoms is characteristic.
2- subacute course - observed in children treated with vitamin D, in children neurological symptoms are less pronounced, damage to internal organs and bone hyperplasia processes predominate.
3- relapsing course - observed under bad conditions
life, poor care, improper feeding, frequent
diseases of the child (ARVI, pneumonia, intestinal
disorders), periods of exacerbation of symptoms alternate
periods of subsidence of the process.
Non-specific treatment
includes organization of the protective regime ,
with the elimination of loud noise, bright light.
Necessary prolonged stay of the child in the fresh air with stimulation of active movements ,
carrying out hygiene procedures - baths or rubdowns.
Diet is built according to age, in addition, from 3-4 months, vegetable and fruit juices, decoctions are given instead of drinking, yolk, cottage cheese are introduced earlier.
Give to improve digestion enzymes - pepsin, pancreatin. Appoint vitamins - C and group B.
An important part of the treatment is
therapeutic gymnastics and massage.
They are held daily for 30-40 minutes.
Spend salt and coniferous baths,
that calm the nervous
system and normalize exchange
processes.
Specific treatment
includes appointment vitamin D
in the form of ergocalciferol (0.125% oil solution or 0.5% alcohol solution), videin or videchol.
With 1 degree of rickets give up to 400,000 IU vit. D
at 2nd degree - up to 600,000 IU
at 3 degrees - up to 800,000 IU
Vitamin is given by the fractional method, those. daily a certain number of drops are dripped onto the root of the tongue or mixed with water or food.
Prevention of rickets:
start prophylaxis in the antenatal period and continue after the birth of the child.
Non-specific prophylaxis includes - observance of the daily routine,
sufficient exposure to fresh air, physical activity, a balanced diet,
prevention and treatment of diseases, massage and gymnastics.
Specific prophylaxis includes
the appointment of ergocalciferol
from 1 month of age,
summer are excluded
An oil solution is given
1 drop
1 per day,
within 1 year.
Conducted periodically
Sulkovich test -
add to 5 ml of morning urine
2.5 ml of Sulkovich's reagent.
The degree of turbidity is judged on the degree of calciuria.
Contraindications for prescribing vitamin D are -
- asphyxia and hypoxia,
- intracranial birth
injury,
- hemolytic disease,
- small size large
fontanel.
Side effects of vitamin D supplements:
Symptoms of vitamin D overdose include:
nausea, vomiting, headache, weakness, irritability, weight loss, intense thirst, frequent urination, kidney stones, soft tissue and vascular calcification.
Spend UV irradiation:
1-2 sessions of 15-20 procedures.
In the initial period of rickets, the level of calcium and phosphorus in the blood decreases Under the influence of parathyroid hormone, the level of calcium usually returns to normal values, while the level of phosphorus remains low Alkaline phosphatase, which is synthesized by hyperactive osteoblasts, enters the extracellular fluid, and its concentration also increases in the blood
Rickets Etiology Endogenous causes: * Violation of absorption processes in the intestine (diarrhea, malabsorption); Violation of the processes of converting vit D into an active form (liver, kidney disease, genetic pathology); Violation of the functional activity of receptors for Vit D (genetic pathology); Rapid growth, increased demand Drug use (antacids, anticonvulsants, loop diuretics, glucocorticoids)
Working classification of Lukyanova E.M. (1988) distinguish: 1) Classical vitamin D-deficient rickets. 2) Vitamin D-dependent rickets associated with a genetic defect in the synthesis of 1,25 (OH) D in the kidneys or with resistance of target organs to it. 3) Vitamin D-resistant rickets (tubulopathy, hypophosphatasia). 4) Secondary rickets in liver diseases, malabsorption syndrome, etc.
Classification of rickets (working classification according to Lukyanova O.M., Omelchenko L.I., Antipkin Yu.G., 1991) Clinical forms Course of the disease Severity Clinical variants st Without significant deviations in the content of Ca and P in the blood
The history of a patient with rickets should include the following: Gestational age, dietary history (detailed nutritional history including questioning of foods containing vitamin D and Ca) length of sun exposure Family history (short stature, bone abnormalities, alopecia, dental problems, consanguineous marriages do not rule out hereditary rickets). Patient examination
Clinical manifestations Garrison's sulcus Harrison's sulcus (E. Harrison, English doctor) deformity of the chest in rickets in the form of a transverse depression located corresponding to the line of attachment of the Harrison groove diaphragm
Concomitant clinical signs of rickets are frequent respiratory infections, iron deficiency anemia of varying severity, latent anemia, changes in other organs and systems (deafness of heart sounds, tachycardia, systolic murmur, atelectatic areas in the lungs and the development of prolonged pneumonia, enlargement of the liver, spleen), the development of conditioned reflexes slows down, and acquired reflexes weaken or completely disappear
The classic radiological triad of rickets Decrease in calcification leads to thickening of the growth zones: "Fringing" of the ends of the metaphyses "Goblet / saucer-shaped" distal sections of the radius, ulna, fibula Expansion of the distal sections and metaphyses
Clinical manifestation of rickets Initial period 1. The first symptoms of rickets are vegetative disorders (age 3-4 months): sleep disorders; irritability; tearfulness; increased sweating: most of the face, scalp; "sour" sweat rubbing the head against the pillow nape baldness; Red dermographism. 2. Compliance of the bones - the edges of the large fontanelle of the small fontanelle of the swept suture, (minor osteoporosis). nape baldness
Peak period Changes in the nervous system, skin Changes in the bone system: 3 months - skull bones; 3-5 months - chest, 6-8 months - limbs; Skull: craniotabes, flattening of the occiput, softening of the bones of the skull, the edges of the fontanelle, an increase in the frontal, parietal tubercles; Thorax: rachitic rosary, deformity of the HA, spine, Harrison's sulcus, looseness of the joints;
Peak period Changes on the part of the bone system: 6-8 months - limbs (O-or X-shaped curvature), pelvic bones; Muscular c-ma: hypotension of the abdominal muscles, frog-like abdomen, lung diastasis - reduced excursion, tachypnea, impaired evacuation function; cardiovascular s-ma - tachycardia, expansion of the boundaries of the heart, tones are weakened; digestive organs - appetite, enzyme activity, flatulence, changes in bowel movements;
Hypophosphatemia - P in the blood (up to 0.48 mmol / l); P in urine - hyperphosphaturia; Hypocalcemia - Ca in the blood (before); Increasing the level of alkaline phosphatase -; Acidosis; Anemia, immunological reactivity; X-ray: osteoporosis, goblet expansion of the metaphyses; peak period
I - mild: changes in the nervous system, bone changes in one part of the skeleton; II - moderate: changes in all organs and systems, changes in two parts of the skeleton III - severe: dysfunction of all organs and systems, changes in three parts of the skeleton The severity of rickets
Type 1 Autosomal recessive Mutation in the gene encoding the renal enzyme 1, hydroxylase, which converts 25-hydroxyvitamin D3 to the active metabolite 1,25-dihydroxyvitamin D3 Occurs in the first 2 years of life Clinical signs are the same as in classic rickets Vitamin D- dependent rickets Type 2 Autosomal recessive Mutation in the gene encoding the vitamin D receptor, which provides a physiological response to the active metabolite 1,25-dihydroxyvitamin D3 Alopecia - 50-70%
Defective gene on the X chromosome, but female carriers of this gene are diseased (X-linked dominant type) Clinical signs: limb deformities, growth retardation - leading symptoms, late teething, dental abscesses, hypophosphatemia Laboratory signs - hyperphosphaturia, hypophosphatemia, alkaline phosphatase, PTH and Ca is the norm. Treatment – P, calcitriol Vitamin D resistant rickets (X-linked hypophosphatemic rickets)
Specific - vitamin D 3: from a week. pregnancy during 6-8 weeks at a dose of - IU / day Indications: pregnant women at risk (preeclampsia, chronic extragenital pathology) 63 Prevention of rickets Antenatal
Specific - vit D 3 Method of fractional doses Full-term healthy children - 500 MO / day, from 2 months. - up to 3 years; Risk group - IU / day from 2-3 weeks of age - 3 years 66 Prevention of rickets Postnatal
Treatment of rickets Vitamin D IU / day for days with the transition to a prophylactic dose
Treatment of rickets Mild - 2000 IU Moderate IU Severe - 5000 IU / day
Treatment of rickets Calcium preparations - Daily dose mg / day calcium glycerophosphate, calcemin 0.1 x 2 times / day, 3 weeks; Products enriched with Ca:
Products enriched with Ca: Orange 35 mg / 100 g product Dried apricots 170 mg / 100 g product Raisins 56 mg / 100 g product Sunflower fruits 100 mg / 100 g product Sesame 1150 mg / 100 g product Milk 1% fat 120 mg / 100 g product Product Milk 3% fat 100 mg/ 100 g Product Cottage cheese 95 mg/ 100 g Product Sour cream 100 mg/ 100 g Product Yoghurt 120 mg/ 100 g Product
Treatment of rickets To normalize the function of the parathyroid glands - magnesium preparations (panangin, asparkam) - 10 mg / kg / day, 3 weeks; To stimulate metabolic processes - potassium orotate - mg / kg / day 20% carnitine hydrochloride 4-12 k. 3 times / day; 1% ATP - 0.5 ml / m 15
slide 2
Presentation plan.
Definition. The incidence rate. The main causes and risk factors for the development of the disease. Methods for the prevention of rickets. Clinical symptoms of rickets by periods. Complications. Classification. Methods of additional diagnostics. Principles of treatment, organization of the nursing process in patient care, principles of dispensary observation. Spasmophilia. Definition. The main causes and risk factors for the development of the disease. Prevention.
slide 3
4. Clinical manifestations of spasmophilia. Complications. Methods of laboratory diagnostics. Principles of treatment. 5. Hypervitaminosis "D". Definition. The incidence rate. The main causes and risk factors for the development of the disease. Prevention.
slide 4
6. Clinical manifestations of hypervitaminosis "D". Complications. Methods of laboratory diagnostics. Principles of treatment. Dispensary observation after an illness in a children's clinic. 7.Organization of the nursing process in rickets, spasmophilia, hypervitaminosis "D".
slide 5
Purpose of the lesson
To form theoretical knowledge on the prevention of the development of rickets, spasmophilia, hypervitaminosis D, early diagnosis of these diseases in children, the basic principles of treatment and the organization of the nursing process in caring for patients.
slide 6
After studying the topic, the student must:
Represent and understand: The role of the nurse in the prevention of diseases under study. Mechanisms of the development of the pathological process in the studied diseases. The role of a nurse in the early diagnosis of rickets, features of the organization of the nursing process.
Slide 7
Know: Causes and risk factors for the development of diseases. Methods for preventing the development of diseases. Early signs and clinical manifestations of diseases, possible problems of patients, diagnostic methods, complications. Principles of treatment and organization of the nursing process in the care of patients. Organization of dispensary observation of children after hypervitaminosis "D" in a children's clinic.
Slide 8
Rickets - A disease that occurs with a violation of all types of metabolism (mainly phosphorus-calcium metabolism, the processes of formation and mineralization of bones).
Slide 9
Manifestations of rickets are more often observed in children aged 2 months to 2 years (from 30 to 35%).
Slide 10
Etiology:
The reasons for the development of rickets can be: insufficient intake from food, malabsorption in the intestines and the formation of vitamin D in the skin under the action of UV radiation (D-deficient rickets); insufficient intake of calcium (Ca-deficient rickets);
slide 11
phosphorus deficiency in the body of a child (P-deficient rickets); insufficient intake with food or impaired absorption and assimilation of protein (protein deficiency rickets); lack of knowledge of parents about the need for measures to prevent the development of rickets; a combination of several causes in one child (polydeficiency rickets).
slide 12
Risk factors for the development of the disease: Perinatal: malnutrition of a pregnant woman (especially calcium deficiency) and violation of the daily regimen; severe preeclampsia and nephropathy of pregnant women; somatic and infectious diseases of the mother; multiple pregnancy; geo-climatic zone of residence;
slide 13
2. Postnatal: prematurity and immaturity of the fetus; unbalanced artificial feeding of a child: the use of unadapted mixtures, the late introduction of complementary foods and corrective additives, predominantly vegetarian feeding; taking anticonvulsants;
Slide 14
insufficient motor activity of the child, lack of massage and gymnastics; hereditary diseases with impaired absorption in the intestine; infectious diseases of the child, especially with prolonged diarrhea; unsatisfactory living conditions, low social level of the child's family.
slide 15
Prevention of rickets
slide 16
Slide 17
Slide 18
Slide 19
Slide 20
slide 21
Vitamin D deficiency decreases the synthesis of Ca-binding protein, which ensures the transport of Ca through the intestinal wall; absorption of Ca in the intestine decreases; Ca leaching from bones Violation of skeletal formation: bones become soft, easily deformed, growth of defective (demineralized) bone tissue occurs in the growth zones.
slide 22
Four periods are distinguished in the clinical course of rickets: Initial period: The first symptoms of the disease appear at the age of 3-4 months, with calcium deficiency - 1.5-2 months.
slide 23
Changes in the nervous autonomic system: the child becomes restless, shy, shudders at sharp sounds and falling asleep; the child's sleep is disturbing, shallow; sweating is pronounced, especially of the face and head, when sucking, in a dream, as a result of which prickly heat often appears on the skin; sweat causes irritation and itching, the child in a dream constantly tosses and turns on the pillow and wipes the hair on the back of the head - baldness of the back of the head appears.
slide 24
Changes in the muscular system: General muscle hypotension; Changes on the part of the skeletal system: Softness and pliability of the edges of the large fontanelle and the sutures of the skull. The duration of the initial period is from 1.5 weeks to 1 month.
Slide 25
Peak period: With untimely diagnosis of rickets and lack of treatment, there is a rapid progression of bone changes, dysfunctions of the nervous and muscular systems, changes appear in the internal organs.
slide 26
Changes in the skeletal system: skull: the edges of the large fontanelle become soft, areas of softening appear along the sutures, softening of the bones of the skull (craniotabes), flattening of the occiput, its asymmetry is noted, almost simultaneously there is an increase in demineralized tissue and the appearance of frontal and parietal tubercles that give the head square shape. A large fontanel closes late (by 1.5-2 years).
Slide 27
Slide 28
Slide 29
slide 30
teeth: they appear late, the order of their eruption is disturbed, there is a tendency to caries due to enamel defects; chest: at the junction of the bone and cartilaginous parts of the ribs, thickenings (costal beads) are formed, the softness of the ribs contributes to the appearance of lateral compression of the chest, the curvature of the clavicles increases, the upper part of the chest narrows, and the lower one expands; in places where the diaphragm is attached, a retraction (Harrison's furrow) is determined, the anterior part of the chest, together with the sternum, can protrude forward ("chicken breast") or recede ("cobbler's chest").
Slide 31
slide 32
spine: kyphosis (rachitic hump), lordosis appear, and a little later - scoliosis;
Slide 33
slide 34
extremities: the epiphyses of the bones of the forearm (“rachitic bracelets”), the phalanges of the fingers (“threads of pearls”) thicken, the deformation of the softened diaphyses of the femur and tibia leads to an X-shaped or O-shaped curvature of the legs, flat feet develop.
Slide 35
slide 36
Slide 37
Slide 38
pelvic bones: pelvic deformities caused by retardation of bone growth, while the entrance to the pelvic cavity narrows, the sacrum and coccyx move forward, the anteroposterior size decreases (flat rachitic pelvis).
Slide 39
Changes in the muscular system: pronounced hypotension of all muscle groups; weakness and flabbiness of the muscles of the abdominal wall leads to an increase in the size of the abdomen (“frog belly”);
Slide 40
there is weakness of the ligamentous apparatus, as a result of which looseness of the joints appears, the range of motion increases (symptom of a "pen" or "folding" knife); there is a delay in motor development (the child later begins to sit, stand, walk).
Slide 41
Slide 42
Changes in the internal organs: respiratory organs: impaired respiratory efficiency due to chest deformation, muscle hypotension, decreased diaphragm contractility (shortness of breath, pneumonia); cardiovascular system: weakening of cardiac tones, tachycardia, systolic murmur, hypotension;
slide 43
digestive organs: intestinal atony (flatulence, constipation, formation of "fecal stones"), dyspeptic disorders, impaired liver function; hematopoietic organs: hypochromic anemia develops, homeostasis disturbance, etc.
Slide 44
The period of convalescence: neurological and vegetative symptoms disappear, the general condition of the child improves, his physical activity increases. Much slower is the normalization of muscle tone and the restoration of static skills. The level of phosphorus in the blood is restored, and the level of calcium remains markedly reduced due to its active deposition in the bones.
Slide 45
The period of residual effects: By the age of 2-3 years, the child has bone deformities, functional changes in the internal organs, biochemical blood parameters gradually normalize.
Slide 46
According to the severity of rickets, it happens: I degree (mild) - there are symptoms of only the initial period; II degree (moderate) - moderately pronounced peak period; III degree (severe rickets) - pronounced musculoskeletal changes, severe damage to the central nervous system and internal organs, delayed physical and psychomotor development, anemia.
Slide 47
Complications:
enamel defects and early caries of milk and permanent teeth; rachitic narrow pelvis, especially in girls; development of persistent bone deformities, violation of posture; high risk of infectious diseases.
Slide 48
Additional methods for diagnosing rickets:
biochemical blood test (hypocalcemia, hypophosphatemia, increased activity of alkaline phosphatase); radiography of the wrists (osteoparosis); Ultrasound (thickening of the epiphyses of tubular bones).
Slide 49
Basic principles of treatment of rickets
Rational nutrition of the child: the maximum duration of natural feeding, in the absence of breast milk - feed the child with adapted mixtures, the introduction of juices, cottage cheese, egg yolk, vegetable puree, buckwheat or oatmeal, meat complementary foods in accordance with the age. Rational day regimen: sufficient stay in the fresh air, sleep in the fresh air, walks in any weather.
Slide 50
3. Specific therapy: - preparations of vitamin "D" (cholecalciferol - D3 and ergocalciferol - D2). In the initial period of rickets, the daily dose is 1500-2000 IU, in the peak period - 3000-4000 IU. The course of treatment is from 30 to 45 days. The criterion for the end of the course of treatment is the normalization of the clinical manifestations of rickets, laboratory parameters. For children at risk (premature, often ill, with malnutrition), the dose of the drug is selected individually. In order to avoid an overdose of vitamin D, it is necessary to periodically examine the urine using the Sulkovich test.
Slide 51
Physiotherapy: UVR 15-20 procedures are prescribed in case of malabsorption in the intestines, in case of impaired absorption of vitamin "D" or after the end of the course of treatment with vitamin "D" preparations. It is impossible to simultaneously carry out treatment with vitamin D and UVI preparations.
Slide 52
4. Non-specific treatment: vitamin therapy: B vitamins, ascorbic acid; calcium glycerophosphate during breastfeeding can be prescribed to the mother 0.5 * 3 times a day for 7-10 days a month; citrate mixture, 1 teaspoon 3 times a day for 1-1.5 months (especially with large doses of vitamin D, since its use allows you to reduce the dose of the drug);
Slide 53
dibazol, prozerin - with severe muscle hypotension; Exercise therapy, massage, therapeutic baths with decoctions of valerian, motherwort (in the initial period and in full swing), salt-coniferous (in the period of convalescence).
Slide 54
Spasmophilia
Slide 55
Spasmophilia is a disease based on hypocalcemia, which causes an increased readiness of the body for tonic and clonic convulsions.
Slide 56
It occurs in children from 3 months to 2 years.
Slide 57
Risk factors for the development of the disease: the appointment of treatment of rickets with large doses of vitamin D (with severe rickets or feeding with unadapted mixtures); hyperproduction of vitamin D in the skin of a child in early spring with increased insolation.
Slide 58
Prevention of spasmophilia is the timely detection and adequate treatment of rickets.
Slide 59
The mechanism of the pathological process
Vitamin "D" increased deposition of Ca in the bones and its slight absorption in the intestine; a critical decrease in the level of Ca in the blood serum (hypocalcemia); hyperphosphatemia; a violation of mineral metabolism and acid-base balance (alkalosis);
Slide 60
The main clinical manifestations of spasmophilia
2 forms of children's tetany: hidden (latent) form; explicit form.
Slide 61
The latent form of the disease often precedes the explicit form and can last from several weeks to several months.
Slide 62
Symptoms: Khvostek's symptom - with a slight tapping with a finger in the cheek area between the zygomatic arch and the corner of the mouth (fossa caninae), the mimic muscles of the corresponding side contract; Lust's symptom - when hitting below the head of the fibula, the foot is rapidly abducted;
Slide 63
Trousseau's symptom - when the neurovascular bundle is squeezed in the middle third of the shoulder, after 3-5 minutes the hand contracts convulsively, taking the position of the "obstetrician's hand"; Maslov's symptom - under the influence of pain irritation (prick), a short-term cessation of breathing occurs.
Slide 64
An obvious form of childhood tetany: Laryngospasm occurs paroxysmal in the form of a slight spasm of the glottis or its complete, short-term closure, accompanied by cyanosis (the child is frightened, covered with sticky sweat), after a short spasm, a noisy breath occurs, reminiscent of a “cock crow”. The attack lasts from a few seconds to 1-2 minutes, during the day it can be repeated.
Slide 65
Carpopedal spasm - tonic contraction of the muscles of the feet and hands; the brushes are maximally bent. The thumb is brought to the palm, the remaining fingers are bent at a right angle in the metacarpophalangeal joints, and in the interphalangeal joints are unbent ("obstetrician's hand"); feet are in a state of sharp plantar flexion.
Slide 66
Eclampsia - the rarest, but most severe form of overt tetany, is a general attack of tonic-clonic convulsions that begin with numbness, lethargy, twitching of facial muscles, convulsions spread to other muscle groups, the child's breathing becomes intermittent, sobbing, cyanosis appears, the child loses consciousness, involuntary urination and defecation occurs. After an attack, the child usually falls asleep. The duration of the attack is from a few to 20-30 seconds.
Slide 67
Complications:
during an attack of eclampsia, respiratory and cardiac arrest may occur; with laryngospasm, sometimes there may be respiratory arrest (death); convulsions of the respiratory muscles with carpopedal spasm.
Slide 68
Diagnostic methods
Biochemical analysis of blood: hypocalcemia, hyperphosphatemia, alkalosis in the blood.
Slide 69
Basic principles for the treatment of tetany
An obvious form of childhood tetany requires urgent measures: create a calm environment around the child; to release him from the constraining clothes; provide sufficient aeration;
Slide 70
Apply methods of tactile stimulation of respiration (to create a dominant focus in the brain): pat on the cheeks and buttocks, sprinkle cold water on the face, irritate the root of the tongue (R-p Ca gluconate per os on the root of the tongue), pressing on it with a spatula, bring to the nose with a cotton ball moistened with ammonia.
Slide 71
as prescribed by the doctor, introduce an anticonvulsant (secuxen, GHB, magnesium sulfate, calcium gluconate); in case of inefficiency, artificial ventilation of the lungs, inhalation of 100% oxygen is used.
Slide 72
Assigned: plentiful drink (tea, berry or fruit juices); a course of treatment with calcium preparations (5% solution of calcium chloride or calcium gluconate); 5% solution of ammonium chloride; 3-4 days after seizures, a course of anti-rachitic treatment with vitamin D preparations
Slide 73
Hypervitaminosis D
Slide 74
Hypervitaminosis D (D-vitamin intoxication) is a condition caused by an overdose of vitamin D or an increased sensitivity of the body to vitamin D preparations, followed by the development of hypercalcemia and toxic changes in organs and tissues.
Slide 75
Risk factors for the development of the disease: uncontrolled intake of vitamin D preparations; an overdose of vitamin D preparations; the appointment of vitamin "D" in the summer;
Slide 76
the use of vitamin D preparations simultaneously with adapted milk mixtures, without taking into account the content of calciferol in them; individual hypersensitivity to vitamin D preparations.
Slide 77
Prevention of hypervitaminosis D
Compliance with the rules for the use of vitamin "D". Individual approach to prescribing vitamin D preparations. Systematic monitoring of the level of calcium in the urine, during treatment with vitamin D, using the Sulkovich test at least 1 time in 2 weeks.
Slide 78
The mechanism of the development of the disease
Hypercalcemia hypercalciuria deposition of calcium in the walls of blood vessels with subsequent irreversible calcification of internal organs affects the organs involved in the activation and excretion of vitamin D (liver, kidneys and the cardiovascular system), impaired mineral metabolism (hypophosphatemia), negative nitrogen balance and acidosis.
Slide 79
II clinical forms of hypervitaminosis D: Acute D-vitamin intoxication: develops in children of the 1st year of life with uncontrolled intake of vitamin D.
Slide 80
Leading symptoms: symptoms of intestinal toxicosis; neurotoxicosis; violation of the functions of vital organs.
Slide 81
Clinical symptoms of intestinal toxicosis: loss of appetite up to complete anorexia, thirst; persistent vomiting, rapid weight loss; development of symptoms of dehydration (dry skin, facial features are pointed, a large fontanel sinks, tissue turgor and muscle tone are reduced).
Slide 82
Clinical symptoms of neurotoxicosis: irritability, followed by lethargy and drowsiness; vegetative disorders (sweating, red dermographism); clouding of consciousness up to the development of coma; convulsions.
Slide 83
From other organs: changes in cardiovascular activity; kidney failure; liver dysfunction; changes in blood parameters (anemia, hypercalcemia, azotemia, acetonemia); bone changes (excessive deposition of calcium in the growth zones of tubular bones).
Slide 84
Chronic D-vitamin intoxication occurs against the background of long-term use of the drug in moderate doses and is characterized by: reduced appetite, vomiting is rare; the weight curve is flattened; there is restless sleep, irritability; rapid fusion of the sutures of the skull and early closure of the large fontanel; on the part of other organs and systems, the changes are expressed insignificantly.
Slide 85
Complications:
acute renal failure, toxic hepatitis, acute myocarditis; early closure of bone growth zones with impaired skeletal development; early development of sclerosis of the vessels of internal organs, a gradual lag in physical and mental development.
Slide 86
Diagnostic methods:
biochemical blood test: hypercalcemia, azotemia, acetonemia; urinalysis: hypercalciuria, hyperphosphaturia; sharply positive test according to Sulkovich.
Slide 87
Basic principles of treatment of hypervitaminosis D
Stop taking vitamin D and calcium supplements. Detoxification therapy: parenteral administration of Hemodez, 5% glucose solution of rheopolyglucin, albumin, Ringer's solution. Introduction of vitamin D antagonists: vitamins A and E.
Slide 88
4. Hormonal therapy (prednisolone to reduce the toxic effect of vitamin "D"). 5. Fight against acidosis (humidified oxygen, parenteral administration of sodium bicarbonate). 6. Removal of calcium preparations (drugs that bind calcium in the intestine - almagel, ksidifon, cholestyramine and drugs that remove calcium from the intestine - trilon B). 7. Symptomatic therapy.
Slide 89
Nursing process in vitamin metabolism disorders
Possible patient problems: malnutrition due to irrational feeding, delay in the appearance of teeth; risk of violation of the integrity of the skin due to hyperhidrosis (risk of prickly heat, etc.); violation of the sleep formula; high risk of infection;
Slide 90
psycho-emotional lability, lag in neuropsychic development; decreased motor activity due to muscle hypotension; decrease in weight and height indicators, lag in physical development; change in appearance due to deformation of the bones of the skeleton; the risk of developing seizures, eclampsia; lack of attention and communication with parents
Slide 91
Possible problems for parents: lack of information about the disease; lack of knowledge about rational feeding, child care; concern about the appearance of the child; fear for the child, uncertainty about the successful outcome of the disease; Fear of an overdose of vitamin "D" due to a lack of knowledge of the rules for the prevention of vitamin "D"; feeling of guilt towards the child.
Slide 92
nursing intervention
Polyclinic nurse: 1. To help parents see the prospects for the development of a healthy child, to fill their lack of knowledge about the causes, course features, prevention, treatment and prognosis of the disease.
Slide 93
2. Consult parents on the organization of rational feeding in accordance with the age and needs of the child: convince the mother to keep breastfeeding the child as long as possible; when introducing complementary foods, use products containing vitamin D (buckwheat porridge, egg yolk, butter and vegetable oil, fish, caviar); from the second half of the year - meat, minced liver;
Slide 94
for children with rickets, it is advisable to cook porridge on a vegetable broth; with artificial feeding, preference should be given to adapted lactic acid mixtures, while taking into account the dose of vitamin D contained in them; limit whole cow's milk in the child's diet as much as possible due to the high content of calcium and phosphates; from 4 months, start introducing freshly prepared juices, fruit and vegetable purees in optimal quantities.
Slide 95
3. Organize a sufficient stay of the child in the fresh air at any time of the year, try to avoid walking in direct sunlight in the spring season, avoid restrictions on the child's physical activity. 4. Recommend sleeping on open verandas (protected from the wind) and in the shade of trees.
Slide 96
5. During the period of wakefulness, stimulate the mental and motor activity of the child, encourage play activities, select toys and games according to age. 6. Recommend parents to regularly conduct courses of therapeutic exercises and massage, teach them the basic techniques in accordance with the age and condition of the child.
Slide 97
7. Teach parents how to conduct therapeutic baths with decoctions of valerian, motherwort in the initial period of rickets and when the child is restless, salt and coniferous baths. 8. Consult parents on the method and technique of giving vitamin D: explain the features of the action and use of oil and alcohol preparations, teach the rules for calculating a single and daily dose in drops, warn against overdose (use only a special pipette, count the drops correctly), vitamin "D" before use, it is preferable to dilute in breast milk, store in a cool, dark place.
Slide 98
9. Help parents to correctly assess the condition of the child, consult a doctor in a timely manner if he develops dyspeptic disorders or changes in behavior. 10. Convince parents of the need for dynamic monitoring of the child by a pediatrician.
Slide 99
Hospital nurse: Carefully perform all manipulations, if possible, exclude invasive interventions. Independent interventions: adherence to the SEP and rules for child care; control over the observance of the rational nutrition of the child; organization of the child's leisure; creating a positive emotional mood; elimination of the lack of knowledge of parents about the disease.
Slide 100
Dependent interventions: giving the child therapeutic doses of vitamin D and other drugs as prescribed by the doctor; interdependent massage, exercise therapy, therapeutic baths.
Slide 101
Sources of information: Textbook Ezhova N.V., pp. 201-212. Textbook by Svyatkina K.A., pp. 39, 99-115. Study guide Sevostyanova N.G., pp. 302-318. Textbook Tulchinskaya V.D., pp. 54-66.
Slide 102
Thank you for your attention!
View all slides
