rickets
Introduction
Introduction to rickets Vitamin D deficiency rickets, referred to as rickets. It is more common in infancy, which is caused by vitamin D deficiency, which causes disorder of calcium and phosphorus metabolism in the body, and causes calcification of bones. The onset of rickets is slow and it is not easy to attract attention. Rickets reduce the resistance of children, and it is easy to combine diseases such as pneumonia and diarrhea, affecting the growth and development of children. Therefore, we must actively prevent it. basic knowledge The proportion of illness: 0.12% Susceptible population: more common in infancy Mode of infection: non-infectious Complications: anemia, chicken breast, funnel chest
Cause
Cause of rickets
Vitamin D deficiency (45%):
Vitamin D deficiency is the main cause of this disease. There are two ways to source Vit D. One is homology. It is converted into cholecalciferol (cholec) by 7-dehydrocholesterol stored in the basal layer of the skin by ultraviolet rays with a wavelength of 296-310 m in sunlight. Alciferol) is vitamin D3 (VitD3). Another way is exogenous, that is, the food intake contains VitD, such as liver containing 15 ~ 50IU / kg1, milk 3 ~ 40IU / L, egg yolk 25IU /. However, the amount of VitD in these foods is very small, which is not enough for the body. The ergosterol forms a vitamin D2 (calcified alcohol, Calciferol) after being irradiated with ultraviolet rays. Both VD2 and VD3 can be artificially synthesized to have the same effect on humans.
Insufficient UV exposure (20%):
Insufficient UV exposure is also a major cause of VitD deficiency, especially in the North. Ultraviolet light is applied to the skin to obtain enough VitD3. China has a vast territory, different natural conditions in the north and south, especially in the sunshine, the length of sunshine is long, the incidence of rickets is low, the sunshine time in the north is short, and the incidence is high. However, ultraviolet rays in sunlight are easily blocked or absorbed by dust, smoke, clothing and ordinary glass. At present, China's industrial development is fast, and there are many urban buildings. In some places, it also brings air pollution. High-rise buildings, light barriers, and living in the home can all affect the ultraviolet radiation.
Overspeed (20%):
There are also more VitDs required. Therefore, children with fast growth are prone to rickets. Premature infants have insufficient calcium and phosphorus reserves, and grow faster after birth. If they lack VitD, they are prone to rickets.
Food factor (5%):
Insufficient calcium or phosphorus in food or inappropriate proportion can also lead to rickets. For example, the proportion of calcium and phosphorus in human milk is suitable, the ratio is 2:1, easy to absorb; while milk contains more calcium and phosphorus, but the phosphorus is too high and the absorption is poor, so the incidence of rickets in milk-fed children is higher than that of human milk. Children are high. Excessive cereals contain a lot of phytic acid, which can combine with calcium and phosphorus in the small intestine to form insoluble phytochemical calcium, which is not easy to absorb.
Chronic disease (5%):
Chronic respiratory infections, gastrointestinal diseases, and liver, pancreas, and kidney disorders can affect VD and calcium and phosphorus metabolism.
Acid and alkalinity are not suitable, and can also affect the absorption of calcium and phosphorus by the intestine. Generally, when the intestinal pH is low, calcium and phosphorus are absorbed more.
Prevention
Rickets prevention
1. Popular precautions
(1) Strengthen publicity work, including reasonable prevention of rickets for pregnant women, perinatal period, and babies, and implement them in the work of maternal and child health management system.
(2) Promotion of legal VitD fortified foods. In recent years, the Nutrition Research Laboratory of Beijing Pediatric Research Institute has developed vitamin AD fortified milk (AD milk), including VitA2000IU/L and VitD600IU/L. It has been proved by experiments that this kind of fortified milk no longer increases VitD preparation, which is to solve the milk feeding child VitA. The lack of VitD and the safest, most effective, convenient and economical way to prevent its overdose has been promoted in Beijing and is worthy of introduction.
(3) Strengthen the reasonable management and feeding of infants and young children, breastfeeding for 8 months, and add food supplements on time.
(4) Strengthen children's outdoor activities, and strengthen the three-bath exercise (air bath, sunbathing, water bath) for group children.
(5) Prevention and early treatment of common diseases in infants and young children.
(6) In the design of the living room by the urban construction department, the angle of sunlight should be taken into account. A greening activity area for children (including the elderly) should be considered in the complex. Or build a children's activity area on the flat roof of the building, especially in the north.
(7) Artificial ultraviolet devices should be introduced into conditional support institutions.
2. Drug prevention law
(1) Emphasis on outdoor activities during pregnancy is not only the prevention of sun-ray ultraviolet rays, but also the benefits of the body. Especially in the third trimester of pregnancy, VitD400IU is supplemented daily in addition to sunshine.
(2) After 1 to 2 weeks in the neonatal period, daily oral VitD400IU, or oral administration of VitD3 to 50,000 IU per day, or oral administration of VitD 10 to 150,000 IU per quarter. Breast milk and milk-fed children's daily diet 400 ~ 500ml does not require calcium, generally calcium is not as easy to absorb and use calcium in milk. In summer and autumn, you can make full use of sunlight. After entering the winter, you should take VitD10~150,000 IU orally, and then return it once every two to three months (that is, the end of winter in the coming year). This method is especially suitable for rural areas for three consecutive years.
(3) Premature infants, double-stage children, and children with digestive tract diseases may be given a slight amount of VitD prevention as appropriate, but should not be excessive to avoid poisoning.
Complication
Complications of rickets Complications Anemia chicken chest funnel chest
The disease mainly causes the baby to look up, sit, stand, walk late, joints are loose and overextended, cerebral cortical dysfunction, conditional reflex formation, language development, anemia and other symptoms.
In some of the more serious cases of rickets, other bone deformations, such as chicken breasts, funnel chest, X-legs, O-legs, ribbed beads, bracelets and anklets.
Symptom
Symptoms of rickets common symptoms joint relaxation osteomalacia osteomalacia curvature of the spine thoracic thoracic deformity flat pelvic bone metabolism reduce neonatal hypophosphatemia renal tubular acidification dysfunction
The child with this disease may have the following symptoms:
(A) mental and neurological symptoms: sweating, night terrors, crying, etc., sweating has nothing to do with the climate, due to sweat stimulation, children often rub the occipital, forming occipital baldness or ring hair loss.
(2) Osteophyte performance.
1, the head.
(1) Skull softening: It is an early manifestation of rickets, which is more common in infants from March to June.
(2) Cranial deformity: "square skull", "saddle head" or "crosshead"
(3) The front is large, the closure is late, and it can be closed until 2-3 years old.
(4) Late teething can be extended to 1 year old teething, or 3 years old, and the teeth are not aligned and the enamel is poorly developed.
2, chest.
(1) The ribs are affected by beads.
(2) Thoracic deformity: chicken chest; funnel chest.
3, limbs and spine.
(1) The wrist and ankle are inflated to form a bangle and a foot bracelet.
(2) Lower limb deformity "O" shaped leg (knee varus), or "X" shaped leg (knee valgus).
(3) curvature of the spine: there may be scoliosis or kyphosis. In severe cases, pelvic deformity (hip valgus) may also be seen. In severe cases, women may become dystocia due to pelvic deformity in adulthood.
(3) Other performances: look up, sit, stand, walk late, joints are loose and overextended, cerebral cortical function is abnormal, conditioned reflex formation is slow, language development is backward, anemia.
Examine
Rickets check
The auxiliary examination methods for this disease are mainly laboratory tests and X-ray examinations:
1. Laboratory inspection:
(1) Alkaline phosphatase appears earlier in the course of rickets, and recovery is the latest, which is conducive to examination and diagnosis.
(2) Determination of serum 25(OH)D3 or 1,25(OH)2D3 levels, the value of which is zero in typical rickets, and also significantly decreased in subclinical rickets, and vitamin D can be significantly increased after treatment, which is sensitive. Reliable biochemical indicators.
2, X-ray inspection:
X-ray changes were evident in long bones with faster bone development, especially at the distal end of the radius and the proximal humerus.
Diagnosis
Diagnosis of rickets
Diagnose based on
The etiology, clinical manifestations, blood biochemistry and bone X-ray examination of blood D deficiency, blood biochemistry and bone X-ray examination are the "gold standard" for diagnosis. The plasma 25-OH-D3 concentration should be 50nmol/L whether infant or child. (20 ng/mL). Early symptoms of increased neurological excitability are not specific,
Differential diagnosis
Need to be identified with the following diseases:
(1) Cartilage malnutrition: It is a hereditary cartilage development disorder. When you are born, you can see short limbs, large head, forehead protrusion, lumbar protrusion, and hip kyphosis. Diagnosis is based on a particular posture (short limb short) and skeletal X-ray.
(2) hypophosphatemia antibiotic D rickets: the disease is mostly sexually linked inheritance, can also be autosomal dominant or recessive inheritance, there are scattered cases. It is caused by the renal tubular reabsorption of phosphorus and the primary defects of phosphorus absorption in the intestine. Symptoms of rickets occur after 1 year of age, so there is still active rickets after 2 to 3 years of age; blood calcium is more normal, blood phosphorus is significantly reduced, and urinary phosphorus is increased. It should be differentiated from this disease when it is not effective in treating rickets with a general therapeutic dose of vitamin D.
(3) distal renal tubular acidosis: for the distal convoluted tubules, hydrogen deficiency, loss of a large amount of sodium, potassium, calcium from the urine, secondary hyperparathyroidism, bone decalcification, signs of rickets. The child has obvious skeletal malformation, short stature, metabolic acidosis, polyuria, alkaline urine, in addition to hypocalcemia, hypophosphatemia, low blood potassium, increased blood ammonia, and often hypokalemia symptoms.
(4) Vitamin D-dependent rickets: autosomal recessive inheritance, which can be divided into two types: type I is a defect of kidney 1-hydroxylase, which causes 25-OH-D3 to become a disorder of 1,25-OH2-D3. The concentration of 25-OH-D3 in the blood is normal; type II is the receptor defect of the target organ, and the concentration of 1,25-OH2-D3 in the blood is increased. Both types of clinical manifestations of severe rickets, hypocalcemia, hypophosphatemia, alkaline phosphatase increased and secondary hyperparathyroidism, type I children may have high amino aciduria; type II An important feature of children is hair loss.
(5) Renal rickets: Chronic renal dysfunction caused by congenital or acquired causes, leading to disorder of calcium and phosphorus metabolism, low blood calcium, high blood phosphorus, secondary hyperfunction of the parathyroid glands, general decalcification of bones, bones It is a disease change. More symptoms than the early childhood gradually became obvious, forming a dwarf state.
