It is one of the most common diseases in infants and children and is clinically common. It is mainly a disorder of calcium and phosphorus metabolism and a disorder of bone development caused by vitamin D deficiency. With the development of society and the improvement of economic level, the incidence of simple vitamin D deficiency rickets has decreased significantly, but vitamin D deficiency rickets is still seen in mountainous areas, some economically underdeveloped areas or due to diseases, among which mild to moderate rickets is most common. It may be related to the local sunshine and less outdoor activities in winter. Etiology: According to the causes, it can be divided into the following two aspects. (1) Insufficient sunlight (1) According to the formation process of vitamin D, it is known that the synthesis of endogenous vitamin D requires ultraviolet radiation from sunlight, which transforms 7-dehydrocholesterol in the body into vitamin D3. If there is insufficient exposure, the synthesis of endogenous vitamin D is reduced, especially in winter, when there is little outdoor exercise and the emphasis on ultraviolet light is weak, it is more likely to lead to this disease. (2) Decrease in exogenous vitamin D intake According to research on dairy products including breast milk, it is found that the vitamin D content in dairy products is low and cannot meet the increasing growth needs of infants and young children, which can easily lead to vitamin D deficiency if reasonable supplementation is not paid attention to. (3) absorption is reduced because the absorption of vitamin D is mainly in the gastrointestinal tract, any gastrointestinal diseases, especially children are prone to viral diarrhea, or even chronic enteritis, which affects the absorption of vitamin D. Other such as drugs can also cause impaired absorption of vitamin D. Second, the need to increase due to early childhood, its growth rate is particularly fast, according to research on child development, in infancy and early childhood, its growth and development is accelerated, leading to an increase in vitamin D, if unreasonable supplementation, leading to the occurrence of rickets. Pathology: mainly abnormal development at the epiphysis of bones, including increased chondrocytes and hypertrophy at the epiphysis and impaired ossification. Under normal circumstances, chondrocytes at the epiphysis increase in size and hypertrophy, then there is capillary invasion, and under the role of local cell regulation, the chondrocyte matrix calcifies, and then after a series of reactions, local ossification and the formation of new bone. If the body is deficient in calcium, the hypertrophic chondrocyte matrix cannot calcify, but the cells in the local cartilage still keep adding value and developing, resulting in thickening of the cartilage layer, increasing local bone-like tissue, widening and enlarging of the epiphysis, and swelling-like changes in the epiphysis. In the long bones of the extremities, the accumulation of large amounts of osteoid tissue leads to the production of hand and foot bracelets. At the rib cartilage, the accumulation of osteoid tissue produces string-like beads, while the bone trabeculae are sparse and disorganized, and the collagen fibers are abnormally aligned. If the patient is weight-bearing early, skeletal distortions, such as internal and external knee deformities, may occur. Once the body is treated and the calcium deficiency is restored, the hypertrophic chondrocyte matrix quickly calcifies and ossifies, the subperiosteal bone-like tissue rapidly calcifies, and under weight-bearing, the bone trabeculae of the body reshape and restore the normal bone growth. Clinical manifestations: 1. General symptoms include drowsiness, noisy crying at night, general muscle weakness, easy to be frightened, excessive sweating, and delayed tooth eruption, etc. 2. Skeletal changes are mainly epiphyseal changes and weight-bearing-induced changes in skeletal shape. These include square skull, thin cranial cortex, large fontanelle, delayed closure; the rib edges on both sides of the chest are turned out, and there are bead-like changes at the rib cartilage joint, as well as the rib cartilage groove, also known as Harrison’s groove, and in severe cases, the thorax is deformed and the development of heart and lungs is imaged; the spine is not obviously changed in general, but in severe cases, there is scoliosis deformity; the limbs are obviously changed In severe cases, there is a deformation of the thorax, imaging the development of the heart and lungs; the spine generally changes inconspicuously, in severe cases there is scoliosis deformity; the limb changes are obvious, in the long bone epiphysis expansion, the formation of hand and foot bracelets, while the long bone distortion caused by weight bearing after calcium deficiency, the formation of O-shaped or X-shaped legs, while there is an abnormal gait. Laboratory tests: 1. alteration of serum 25-OHD Due to vitamin D deficiency, the deficiency of serum 25OHD, which decreases as the disease progresses, is positively altered. 2. biochemical examination main indicators include elevated alkaline phosphatase, increased urinary phosphorus, low blood calcium, low blood phosphorus. 3. increased blood parathyroid hormone. 4. decreased bone density, etc. Imaging manifestations: mainly X changes. Including the abnormality of the bone itself and the change of appearance, the bone is the earliest to appear with the change of the wrist bone. In severe cases, the entire epiphysis is changed in a burr-like manner, the bone cortex is thin, the bone is sparse, and the bone trabeculae are disorganized. The appearance of changes such as internal and external knee deformity, serious scoliosis, etc. Diagnosis and differential diagnosis: The diagnosis is mainly based on the patient’s medical history, including low sunlight exposure, simple dairy feeding, no timely addition of vitamin D, physical signs and clinical manifestations, as well as laboratory tests and X-ray examinations. Differential diagnosis 1. other causes of skeletal developmental changes; 2. chondrodysplasia Patients may have some of the symptoms of rickets, such as large head and chest, but chondrodysplasia also has short stature, asymmetric limb development, normal blood calcium and phosphorus examination. x-ray examination may have specific epiphyseal changes, etc. 3. other causes of rickets, such as A, low blood phosphorus anti-vitamin D rickets Patients mostly have a family history of hereditary disease Most of the patients have a family history of rickets, mostly sex-linked inheritance, mainly primary renal tubular reabsorption of phosphorus disorder and intestinal absorption of phosphorus disorder. B. Distal renal tubular acidosis is mainly due to insufficient hydrogen secretion by the body, which compensates for increased calcium excretion and leads to a decrease in blood calcium, and the body mobilizes parathyroid hormone to decalcify bone and increase blood calcium, resulting in rickets. C. Vitamin D-dependent rickets is also a family genetic disease, mainly due to 1-hydroxylase deficiency, resulting in impaired synthesis of active vitamin D or lack of receptors for active vitamin D in the body, resulting in impaired absorption of calcium and phosphorus in the body, lower blood calcium and phosphorus levels, and symptoms of calcium deficiency, and treatment should be symptomatic according to the cause Treatment should be symptomatic according to the cause. Treatment and prognosis: 1. Prophylactic vitamin D supplementation As infants and young children mainly rely on breast milk and dairy products, while going out to receive sunlight for a short period of time, they need routine vitamin D supplementation, usually 400 units per day, and oral calcium gluconate supplementation, and for premature infants, their vitamin D needs are greater, both to meet the needs of growth and for body reserves. 2, mild rickets Can be given oral vitamin D 1000-2000 units. Moderate to severe can be increased to 4000-6000 units, while supplementing calcium. Orally for about a month, the condition is stable, change to calcification prevention amount of treatment. 3.Blitz therapy is mainly used for those who can not adhere to it every day Can be given 100,000 units orally at once (mild) moderate to severe can be increased to 200,000-300,000 units, only once; or give injections of vitamin D, the main number of times, usually 1-2 times, the condition is stable change to oral treatment, along with the application of calcium. 4.If there is severe knee Internal derangement, after conservative treatment, there is still obvious deformity, can be switched to osteotomy treatment when the bone is mature, the prognosis is good.