Rickets in children

Rickets in children

It mainly occurs in infants under 2 years old. Vitamin D deficiency and metabolic abnormalities are important causes. Nutritional vitamin D deficiency is the main cause.

1. Definition of rickets

A systemic chronic disease caused by vitamin D deficiency, which leads to calcium and phosphorus metabolism disorders (abnormalities) and bone lesions.

2. Common causes of rickets:

1. Insufficient vitamin D storage during fetal period.

2. Insufficient sunlight.

3. Insufficient vitamin D intake after birth.

4. Poor absorption of vitamin D due to illness, medication, etc.

5. Growth and development are too rapid, and the need for vitamin D increases.

6. The calcium and phosphorus content in food is too low or the food is not properly matched.

7. Premature birth or twins.

8. The geographical environment of growth.

3. Clinical manifestations of rickets

1. Initial stage (usually 3-6 months):

Night terrors, sweating, irritability, and baldness on the back of the head may occur. Some people may also experience symptoms such as pallor, abdominal distension, muscle relaxation, and weakness.

2. The stimulating period (usually before 2 years old):

In addition to the initial symptoms, other bone changes such as skull softening may occur, such as square skull, bracelets on hands (foots), rib beads, costal cartilage grooves, pigeon chest, O-shaped legs or X-shaped legs.

3. Recovery period (usually before 2 years old):

Through treatments such as sun exposure and vitamin D supplementation, the symptoms and signs of most children in the early and intense stages (some books call the intense stage the active stage) can gradually be alleviated and disappear.

4. Sequelae period (mostly after 2 years old):

After treatment, the symptoms disappear and bone changes no longer progress, but some children will have varying degrees of bone deformities.

4. Diagnosis of rickets

1. Clinical manifestations

2. Unique physical signs

3. Laboratory examination

(1) During the acute phase of X-ray film, the temporary calcification zone becomes blurred and disappears, the epiphyseal end becomes wide or cup-shaped, the edges are irregular and appear to be "cloudy" or "brush-shaped", and the epiphyseal cartilage becomes widened. During the recovery phase, the temporary calcification zone reappears, becomes wider, and becomes denser.

(2) Acute phase: blood calcium, blood phosphorus, serum 25-(OH)D decrease, AKP increases. Recovery phase: blood calcium, blood phosphorus, serum 25-(OH)D, AKP gradually return to normal.

5. Treatment of rickets

1. General treatment: Strengthen care, get regular sun exposure; adjust the dietary structure and increase the intake of foods high in calcium.

2. Supplement vitamin D to improve serum vitamin D levels. During the stimulation period, vitamin D is 2000-4000∪/day, taken orally once a day. After 1 month, change to 400-800∪/day. Large-dose shock therapy can also be used. That is: vitamin D 150,000-300,000∪/day, intramuscular injection. After 1 month, vitamin D 400-800∪/day, taken orally.

3. Other treatments: supplementation of calcium, vitamins, etc.

4.Surgical treatment (for severe deformity).

Appendix: Precautions for sunbathing

1. Do not expose to direct sunlight or through glass (because ultraviolet rays cannot pass through glass).

2. Choose a suitable time period, preferably between 9:00 to 10:30 a.m. and 3:30 to 5:00 p.m.

3. The time should be increased gradually from short to long. Generally, each session should be ≥ 30 minutes and ≤ 2 hours. It can be done once in the morning and once in the afternoon.