Clinical manifestations: The main manifestation is the ossification of the skeletal system is incomplete or softening of the bone change health search, such as fontanelle enlargement cranial suture widening and posterior fontanelle connected to the side fontanelle is not closed, the edge of the skull and the parietal bone parietal nodal part become soft or ping-pong sense, the edge of the skull especially the parietal bone sagittal suture edge has jagged bone missing missing huge in front of the posterior fontanelle can form a pseudo fontanelle when respiratory distress easy to form funnel chest, premature babies easy to have spontaneous rib Fracture; weight and day-old newborns can also have typical bone like tissue hyperplasia such as rib bead bracelet and square skull. Hypocalcemia in the neonatal period, especially in late neonates, should be considered a possibility of rickets, and older children may also have symptoms such as bald rings and nervous excitement Complications: easy to complicate spontaneous fractures, skull and sternum and other skeletal deformities, and prone to infectious diseases and diarrhea, the formation of neonatal hypocalcemia, can occur in convulsions or laryngospasm, and even cause death. Laboratory tests: normal newborns have high blood phosphorus and low blood calcium in the first week after birth. In neonatal rickets, both blood calcium and phosphorus are reduced, but in some cases, blood phosphorus can be normal or even increased if only blood calcium is reduced, but alkaline phosphatase is mostly increased in the neonatal period due to cholestasis and other non-bone derived alkaline phosphatase is also common, which can affect the judgment of rickets. In rickets, blood 25-(OH)D3 and/or 1,25-(OH)2D3 may or may not be decreased. These biochemical changes do not necessarily parallel the radiographic changes of neonatal rickets. Individual children may have amino aciduria. When neonatal hypocalcemia occurs, there may be a decrease in blood calcium and a decrease in free calcium. Other ancillary tests: The diagnosis of neonatal rickets relies heavily on x-ray examination. The typical infantile rickets X-ray changes can also be seen in the neonatal period, such as generalized skeletal laxity, decreased bone density, thinning of bone trabeculae, thinning of the bone cortex and thinning of the skull cap; widening of the long bone epiphysis, blurring and widening of the temporary calcification zone, with uneven cloud-like or brush-like edges, and cup-like depression of the nucleus pulposus, and widening of the distance between the epiphysis. Usually when a chest x-ray is taken, accidental rickets similar to those seen in rickets of the long bone epiphysis and sometimes spontaneous fractures are found at the rib cribriform junction. In full-term infants, congenital rickets should be considered when the nucleus of the distal femur or proximal tibia is not present. x-ray findings can be divided into 3 stages: 1. the initial ulnar epiphysis is blurred, the bone cortical density is slightly reduced, and the radial changes are slight or absent. 2, Radical phase I ulnar epiphysis is blurred, gross more obvious, and density is reduced, and radial epiphysis is blurred and density is reduced. 3.Blurred and gross ulnar radial epiphysis in radical phase II, temporary calcification zone disappeared and bone density was obviously reduced. Related tests: amino acids; alkaline phosphatase Treatment: Treatment with vitamin D preparation, oral 5000 U per day for 1 month, review X-ray and biochemical changes if improvement is seen then reduce the amount by half for another 1 to 2 months. If the disease is serious, the onset is rapid, there is a funnel chest and so on, the dose can be increased or even with surprise therapy, intramuscular injection of vitamin D3 or D2, each time 50,000 U/kg, once a month for a total of 1 to 3 times. Calcium supplementation of 100 mg/kg per day has been used in some children who have not been treated with vitamin D alone and have been cured with calcium supplementation. Premature infants were fed with modified and fortified preterm formula. Prognosis: Prompt diagnosis and treatment will result in a good prognosis. Attention should be paid to the prevention and treatment of rickets throughout infancy and early childhood to avoid recurrence. Prevention: Prevention of congenital rickets should start from the second trimester of pregnancy. 1. Starting from the 28th week of pregnancy, give pregnant women vitamin D, 1000 U/d, and continue to take it after the birth of the child. 2.Strengthen pregnancy care, pay attention to nutrition, frequent outdoor activities and increase the time of sunlight exposure. 3, actively prevent and treat maternal diseases, such as prevention of hepatitis B, protection of kidney function, etc., so as not to affect the metabolism of calcium, phosphorus and vitamin D in the body late in pregnancy plus vitamin D 50,000 U per month. 4, the current tendency is to increase the amount of vitamin D prevention for newborns, especially premature babies, from the second week after birth, vitamin D can be given 800 to 1200 U per day, but be careful not to exceed the dose of vitamin A 1 10,000 U per day.