How to treat rickets X-type legs?

Written by Li Jiao Yan
Neonatology
Updated on October 25, 2024
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If rickets presents with an X-shaped deformity, it generally indicates either an active phase of the disease or the residual phase. During this time, it is advisable to minimize the child's standing and walking at home. For lower limb deformities, muscle massages can be performed. For X-shaped legs, massage the inner muscle groups, followed by internal rotation exercises after massaging the double sliding joints. Typically, early treatment involves corrective rehabilitation techniques, and it is possible to visit a pediatric rehabilitation department for relevant manual treatments. If there is a significant skeletal deformity, surgical intervention may be necessary for correction.

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Written by Li Jiao Yan
Neonatology
1min 25sec home-news-image

Early symptoms of rickets

Rickets is a chronic systemic nutritional disease caused by insufficient vitamin D in the body, leading to disturbances in calcium and phosphorus metabolism, characterized by skeletal lesions, typically presenting as incomplete mineralization of the long bones' growth plates and bone tissue. In the early stages of rickets, skeletal development abnormalities are not very obvious. Infants under three months often exhibit signs of increased neural excitability, such as being prone to crying, sweating easily, and potentially frequent head shaking; however, these symptoms are not necessarily specific to rickets. Generally, at this time, there are no obvious abnormalities in skeletal development, and X-rays of the bones are normal. The focus is on vitamin levels, specifically decreased serum 25-hydroxy vitamin D, as well as reduced blood calcium and phosphorus levels. Therefore, early symptoms are not so typical. It is recommended that children regularly visit pediatric clinics for physical examinations to assess their development and, if necessary, undergo trace element and vitamin D level checks.

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Written by Li Jiao Yan
Neonatology
1min 37sec home-news-image

What is the treatment method for rickets?

Rickets is primarily caused by a deficiency in vitamin D, leading to disturbances in calcium and phosphorus metabolism in the body, which results in abnormal skeletal development—a type of systemic nutritional disease. The most common form is nutritional rickets due to a deficiency in nutrients and vitamin D. Treatment focuses on controlling the active phase to prevent relapse of deformities. Therefore, early detection and comprehensive treatment are crucial. The primary treatment method involves supplementing with vitamin D. The choice of vitamin D, the dosage, and the length of treatment generally need to be tailored to the specific circumstances of the child. Additionally, increased exposure to sunlight and appropriate outdoor activities should be encouraged to enhance the absorption of vitamin D. Children should also be supplemented with calcium and a variety of vitamins. Follow-ups during the recovery phase are necessary, and training in sitting, standing, and walking should not be started too early to avoid deformities in the lower limbs. Furthermore, no medication is needed during the residual stage of the disease. For mild to moderate cases, physical exercise should be intensified, and skeletal deformities can be corrected using active or passive exercises. Severe skeletal deformities may require surgical correction.

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Written by Yan Xin Liang
Pediatrics
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Does rickets have a hereditary component?

Rickets, also known as vitamin D deficiency rickets, is primarily a chronic nutritional disease characterized by skeletal lesions, caused by insufficient vitamin D in infants, children, or adolescents, which leads to disturbances in calcium and phosphorus metabolism. The main feature of this disease is the incomplete calcification of the growth plates and bone tissue in the growing long bones, due to the lack of vitamin D causing incomplete calcification of mature bones. This disease is most common in children under two years old. Its causes may be related to insufficient intake of vitamin D or insufficient sunlight exposure, as well as rapid growth. Additionally, other diseases may influence its development. Therefore, this disease is generally not closely related to genetics.

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Written by Li Jiao Yan
Neonatology
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Rickets Causes

Rickets, fully termed as nutritional vitamin D deficiency rickets, is a chronic systemic nutritional disease characterized by epiphyseal lesions, caused by insufficient vitamin D in children, leading to disordered calcium and phosphate metabolism. The main causes of the disease include insufficient perinatal vitamin D, particularly during the prenatal and postnatal periods, as well as factors like severe maternal malnutrition, liver and kidney diseases, chronic diarrhea, prematurity, and having twins, which may lead to inadequate levels of vitamin D storage in the body. Additionally, insufficient sunlight exposure, such as children spending prolonged periods indoors, blocks sunlight, as ultraviolet rays cannot pass through glass. Ultraviolet light aids in the synthesis of endogenous vitamin D; lack of exposure can also reduce vitamin D levels. Another factor is rapid growth rates, and fourthly, insufficient dietary supplementation of vitamin D along with some diseases that affect the absorption of vitamin D, like gastrointestinal or liver and biliary diseases.

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Written by Li Jiao Yan
Neonatology
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Rickets symptoms

Rickets, also known as nutritional vitamin D deficiency rickets, is a chronic nutritional disease in children caused by inadequate vitamin D in their bodies, leading to disorders in calcium and phosphorus metabolism and characterized by changes in the growth plates. Its manifestation varies with different ages. In infants under six months, especially those under three months, symptoms often include increased nervous excitability, such as being easily irritable, restless, sweating, and shaking their heads due to scalp irritation. As the condition progresses in children under six months, the primary changes are seen in the skull; the edges of the anterior fontanelle are softer, and the skull is thinner. After six months, the softening of the skull disappears, but there can be ping-pong ball-like changes around the skull, leading to a box-shaped head from seven to eight months. Gradually, beading changes form, most notably around the 7th to 10th ribs. Around the age of one, children can develop a pigeon chest deformity, and in severe cases of rickets, a horizontal depression forms at the lower edge of the thoracic cage, known as the costal groove or Harrison's groove. Due to bone softening and muscle and joint laxity, when the child begins to stand and walk, the legs may become bow-legged or X-shaped, and in severe cases, can develop into 'K'-shaped leg deformities. Once the child starts to sit and stand, general ligament laxity can cause spinal deformities. Severe hypophosphatemia leads to muscle carbohydrate metabolism disorder, resulting in overall muscle laxity, decreased muscle tone, and subsequently reduced muscle strength.