Vitamin D (VitD) deficiency rickets, or rickets for short, is a chronic nutritional disease of the whole body characterized by skeletal lesions caused by abnormal calcium and phosphorus metabolism in the body due to VitD deficiency, resulting in incomplete mineralization of bone tissue during the growth period. Rickets not only affects the normal growth and development of children, but also is related to VitD deficiency-related diseases, and is one of the four diseases that are the focus of pediatric prevention and treatment in China.
The clinical manifestations of rickets include non-specific symptoms, characteristic skeletal changes and other systemic changes.
The active phase of rickets is divided into early, radical, recovery and sequelae phases.
1. Early stage: It is mostly seen in infants less than 6 months old (especially within 3 months old). There may be non-specific neuropsychiatric symptoms such as excessive sweating, occipital baldness, irritability, and night terrors. There are often no skeletal lesions at this stage. Blood calcium and phosphorus are normal or slightly low, alkaline phosphatase (AKP) is normal or slightly high, and blood 25-(OH)D is decreased. There is no abnormality in the long bone epiphysis on bone x-ray or temporary calcification zone is blurred and thinned, and the epiphysis is slightly widened.
2. Radical phase: Skeletal signs: for <6 months old infants, signs of cranial softening (ping-pong sensation) are seen; for >6 months old infants, signs such as square skull, hand (foot) bracelets, rib crossties, rib cartilage grooves, chicken chest, 0-leggedness and x-leggedness are seen. Blood calcium is normally low or decreased, blood phosphorus is significantly decreased, and AKP is increased. Blood 25-(OH)D and 1,25-(0H)2D were significantly decreased. Widening of the long bone epiphysis on bone x-ray, disappearance of temporary calcification zone, brush-like or cup-shaped, widening of epiphyseal cartilage disc >2mm.
3.Recovery period: Early or active children with symptoms disappeared after sunlight exposure or treatment, and the signs gradually reduced or disappeared. Blood calcium, blood phosphorus, AKP, 25-(0H)D, 1,25-(0H)2D gradually return to normal. Temporary calcification zone of the long bone epiphysis reappears, widens and increases in density on bone x-ray, and the epiphyseal cartilage disc <2mm.
4. Posterior period: Mostly seen in children after 3 years of age, due to severe rickets in infancy and childhood, different degrees of skeletal deformities can be left behind. In addition to skeletal lesions, VitD deficiency may also affect other tissues and organs, delaying motor development, such as muscle relaxation and reduced muscle strength (muscle tone); and recurrent infections due to decreased immune function.
VitD deficiency in children may be associated with certain chronic diseases in adulthood, such as diabetes, asthma, multiple sclerosis, etc. VitD deficiency risk factors, clinical signs and symptoms help to diagnose, confirming the diagnosis requires blood biochemistry, bone x-ray radiographs. Serum 25-(0H)D is the best indicator of VitD nutritional status and should be carried out gradually.
The treatment aim is to control the disease and prevent skeletal deformity, and the principle of treatment is mainly oral. the choice of VitD preparation, dose size, duration of treatment, single or multiple doses, and route (oral or intramuscular) should be determined according to the specific situation of the child, emphasizing individualized administration. When the dose is 2000-000U/d (50-100ug/d), it is changed to 400U/d (10ug/d) after 1 month. When absorption is affected by oral administration difficulties or diarrhea, etc., high-dose blitz therapy can be used with VitD 150,000-300,000 U (3.75-7.5 mg)/time, intramuscularly, and then VitD is maintained at 400 U/d (10ug/d) after 1 to 3 months. Follow-up should be done after 1 month of medication. If symptoms, signs and laboratory tests do not improve, other diseases should be considered and differential diagnosis should be paid attention to, and hypercalcemia, hypercalciuria and VitD overdose should be avoided.
Other treatment
1. Calcium supplementation: Milk is a reliable source of calcium nutrition for infants and children, and calcium supplementation is generally not required for rickets treatment.
2. Micronutrient supplementation: attention should be paid to the intake of other multivitamins.
3.Surgery: Severe skeletal deformity can be surgically corrected deformity.
Prevention: The occurrence of rickets is closely related to poor lifestyle. Rickets can be completely prevented and controlled through the comprehensive prevention and control measures of scientific child-rearing. The prevention of rickets should start from the perinatal period, with the focus on infants within one year of age, and should be managed systematically until the age of three. In other words, we should “grasp early, grasp small, grasp thorough”.
(I) Comprehensive prevention and control measures
Special emphasis is placed on the importance of involving parents and caregivers. Make use of various forms of propaganda to widely publicize scientific child-rearing and health knowledge of rickets prevention and control, correct poor child-rearing methods, and guide parents to participate in scientific health care.
(II) Systematic management
Carry out health care management for pregnant women, newborns and infants through maternal and child health care network, and conduct regular follow-up visits and monitor rickets prevention and treatment according to the plan.
(III) Strengthening nursing care
Parents are instructed to provide proper health care and nursing care for children of all ages, regular vaccinations, and active prevention of acute and chronic diseases such as upper respiratory tract infections, pneumonia, diarrhea, and anemia. Reasonable feeding, balanced diet and changing bad habits such as partial eating are very important to prevent rickets.
(iv) Prevention during mother’s pregnancy
Pregnant women should be active outdoors frequently and eat foods rich in calcium and phosphorus. Women whose second trimester is autumn and winter should take appropriate VitD supplements of 400-1000 U/d (10-25ug/d). If available, pregnant women should monitor blood 25-(OH)D concentrations in the second trimester of pregnancy, and if there is significant VitD deficiency, VitD should be supplemented to maintain 25-(0H)D levels in the normal range. VitA and D preparations should be used to avoid VitA toxicity and VitA intake
(E) Infants and children prevention
1, outdoor activities: parents are instructed to bring their infants to outdoor activities as early as possible, gradually up to 1~2h/d, exposing infant body parts such as head and face, hands and feet as much as possible.
2. VitD supplementation: Infants (including exclusively breastfed children) should receive 400 U/d (10 buckets of g/d) of VitD for 2 weeks after birth until 2 years of age, and VitD supplementation should include the VitD content in food, sunlight exposure, VitD preparations, and VitD fortified foods. If infants consume 500″ of formula daily, they can take in about 200u (5ug) of VitD, and with proper outdoor activities (especially in summer when there are more outdoor activities), there is no need to supplement VitD preparations.
3. Supplementation for high-risk groups: Premature babies, low birth weight babies, and twin babies should be supplemented with VitD 800-1000U/d (20-25ug/d) immediately after birth, and 400U/d (10ug/d) after 3 months.