The main manifestations of rickets in the acute stage

Rickets is a very common disease. The formation of this disease is mainly due to the lack of vitamin D in the body, which leads to a decrease in calcium in the body and ultimately causes bone lesions. Rickets is common among children. Many children suffer from rickets since childhood. This disease has a great impact on children's lives. So, what are the main manifestations of rickets in the acute stage?

Rickets, whose full name is nutritional vitamin D deficiency rickets, is a systemic chronic nutritional disease characterized by bone lesions caused by insufficient vitamin D in children, which leads to calcium and phosphorus metabolism disorders. Infants and young children, especially young babies, who grow fast and have little outdoor activities, are a high-risk group for developing nutritional vitamin D deficiency rickets. Causes:

1. Vitamin D deficiency during the perinatal period

Vitamin D deficiency in the mother during pregnancy, especially in the late pregnancy, such as severe malnutrition of the mother, liver and kidney disease, chronic diarrhea, premature birth, and twins can all lead to insufficient storage in the baby's body.

2. Insufficient sunlight

Because ultraviolet rays cannot pass through glass windows, infants and young children are kept indoors for too long, resulting in insufficient endogenous vitamin D production. Tall buildings in big cities can block sunlight, and air pollution such as smog and dust can absorb some ultraviolet rays. Climate influences, such as short daylight hours and weaker ultraviolet rays in winter, can also affect the production of some endogenous vitamin D.

3. Fast growth

Premature babies and twin babies grow and develop quickly after birth, need more vitamin D, and have insufficient vitamin D stored in their bodies, so they are prone to nutritional vitamin D deficiency rickets. Severely malnourished infants have slow growth and few develop rickets.

4. Insufficient vitamin D in food

Because natural foods contain little vitamin D, even babies who are exclusively breastfed are prone to rickets if they do not have much outdoor activity.

5. Impact of diseases

Gastrointestinal or hepatobiliary diseases affect the absorption of vitamin D, such as infantile hepatitis syndrome, congenital biliary stenosis or atresia, steatorrhea, pancreatitis, chronic diarrhea, etc. Severe damage to the liver and kidneys can lead to vitamin D hydroxylation disorders and insufficient production of 1,25-(OH)2D, causing rickets.

Clinical manifestations of rickets

1. Generally speaking, this disease occurs in infants and young children, especially infants under 3 months old.

The main manifestations are bone changes in the fastest growing parts, and can affect muscle development and changes in nerve excitability. Therefore, the clinical manifestations are different at different ages. The bone changes of rickets often appear after a period of vitamin deficiency. Infants with perinatal vitamin D deficiency will develop rickets earlier. Rickets rarely occurs in childhood. Children with severe rickets may also have digestive and cardiopulmonary dysfunction, and their behavioral development and immune function may be affected.

2. Early stage

It is more common in infants under 6 months old, especially in infants under 3 months old. Most of them are manifestations of increased nervous excitability, such as irritability, restlessness, excessive sweating that irritates the scalp and causes shaking of the head. However, these are not specific symptoms of rickets and are only used as a reference for early clinical diagnosis. There are usually no bone lesions at this stage, and bone X-rays may be normal or the calcification bands may be slightly blurred; serum 25-(OH)D3 decreases, PTH increases, blood calcium decreases, blood phosphorus decreases, and alkaline phosphatase is normal or slightly elevated.

3. Active period (stimulation period)

If infants with early vitamin D deficiency are not treated, their condition will continue to worsen, and they will develop typical skeletal changes with PTH hyperfunction and abnormal calcium and phosphorus metabolism. Rickets in infants under 6 months old is mainly characterized by skull changes, with a soft anterior fontanelle and a thin skull. The examiner uses both hands to fix the infant's head and presses the back of the occipital bone or parietal bone with a little force with the fingertips, which may feel like pressing a ping-pong ball. After 6 months of age, the skull softening disappears, although the disease continues to progress. Normal babies may also have a ping-pong ball-like feeling around the bone joints. The central part of the frontal bone and parietal bone often gradually thickens, and by 7-8 months, it becomes a "box-like" head shape (looking from top to bottom), and the head circumference is also larger than normal. A "box-like" head should be distinguished from a head with a wide forehead. The epiphyseal ends swell due to the accumulation of bone-like tissue, and a round protrusion can be seen at the junction of the ribs and costal cartilages along the rib direction. From top to bottom, it is like a string of beads, which is most obvious on the 7th to 10th ribs. It is called rachitic rosary. Blunt round ring-shaped protrusions can also form on the wrists and ankles, which are called bracelets and anklets. Chest deformity can be seen in children around one year old, with the sternum and adjacent cartilage protruding forward to form a "pigeon chest" deformity. In children with severe rickets, a horizontal depression forms at the lower edge of the chest, namely the costophrenic groove or Harrison groove. Sometimes the rib margins on both sides of the thorax of a normal child are slightly higher and should be distinguished from the costophrenic groove. Due to osteomalacia and muscle and joint relaxation, when children start to stand and walk and bear weight on both lower limbs, the femur, tibia, and fibula may bend, resulting in severe knee valgum ("O" type) or knee valgum ("X" type).