How should children with rickets supplement calcium?

Written by Li Jiao Yan
Neonatology
Updated on March 18, 2025
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Rickets is a nutritional disease caused by a deficiency in vitamin D, leading to disturbances in calcium and phosphorus metabolism in the body, which results in abnormal bone development. It is mainly due to a lack of vitamin D, so the primary treatment is supplementing with vitamin D. Dairy is a reliable source of calcium nutrition for infants, and generally, it is not necessary to supplement calcium for the treatment of rickets; attention should be paid to supplementing with vitamin D according to the severity of the condition, and spending more time in the sun. For children who have started eating complementary foods, or older children, it is generally recommended to fully supplement vitamin D levels, spend more time in the sun during summer, and consume high-protein nutrients. Additionally, eating more vegetables and appropriately supplementing with calcium supplements in the winter is advised. The dosage should be based on the child's internal levels of calcium and phosphorus, with calcium supplementation adjusted accordingly.

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Written by Li Jiao Yan
Neonatology
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How to diagnose rickets?

Rickets is caused by a deficiency of vitamin D, which leads to abnormal calcium and phosphorus metabolism, and thus abnormal bone development. Generally, rickets requires biochemical blood tests and vitamin D level assessments, followed by skeletal X-ray examinations. However, some cases of rickets are caused by other special reasons, such as abnormalities in liver and kidney functions, and there may also be congenital genetic diseases. Therefore, rickets also requires further related examinations, such as liver function tests, kidney function tests, and parathyroid hormone tests, and even some genetic level examinations might be conducted.

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Written by Mo Ming Hua
Pediatrics
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If rickets is not treated, what will be the impact?

Rickets, if untreated, mainly involves changes in skeletal deformities and motor function in children. Rickets is primarily caused by a deficiency in vitamin D, which is essential for promoting the absorption of calcium. A deficiency in vitamin D leads to reduced calcium absorption. Lower calcium absorption results in a calcium deficiency in the body, which in turn causes changes in the bones. In the early stages of vitamin D deficiency, the main symptoms are increased neural excitability, which may manifest as startle reactions, irritability, restlessness, and excessive sweating. During the active phase, symptoms of increased nervous system excitability become more pronounced, mainly presenting as skeletal deformities. What aspects do these skeletal deformities affect? One is the softening of the skull, pigeon chest, funnel chest, and changes resembling wristbands and anklets. If the condition worsens further, it can present as X-shaped legs, O-shaped legs, and spinal deformities. Thus, if rickets progresses, it can lead to skeletal deformities and impairments in motor functions, among other issues.

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Written by Zeng Hai Jiang
Pediatrics
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The difference between rickets and rib flare

Rickets and rib flaring are different; rib flaring can be considered a symptom of rickets. Rickets is caused by a deficiency of vitamin D in infants and children, leading to abnormal metabolism of calcium and phosphorus, which results in incomplete calcification and softening of the bones, thereby causing skeletal deformities. Rickets can be divided into initial, active, recovery, and sequelae stages. During the active stage of rickets, skeletal deformities such as softened skull, "ping pong" head, square skull, rib flaring, pigeon chest, funnel chest, X-shaped legs, and O-shaped legs are prone to occur.

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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.

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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.