neonatal rickets
Introduction
Introduction to neonatal rickets Neonatal caries (ricketsofnewborn) is a disorder of calcium and phosphorus metabolism caused by vitamin D and/or calcium phosphate deficiency, and causes growth of skeletal bone matrix calcium salt deposition disorder and/or bone-like tissue (uncalcified bone matrix) A nutritional metabolic bone disease that accumulates into histological features. If the disease has occurred at birth, it is called congenital rickets (CR), also known as fetal rickets, viviparous rickets, etc., neonatal rickets are easy to be associated with low calcium sputum, because the throat can be life-threatening or lacking Oxygen brain damage, therefore should be actively prevented. basic knowledge The proportion of illness: 0.001% Susceptible people: children Mode of infection: non-infectious Complications: diarrhea, neonatal hypocalcemia, neonatal seizures, convulsions in children, throat
Cause
Causes of neonatal rickets
Insufficient storage of calcium, phosphorus and vitamin D (20%):
The calcium and phosphorus of the fetus are from the mother. 75% of the calcium and phosphorus reserves are stored in the last 3 months of pregnancy, that is, after 28 weeks of gestational age, and the intake reaches the highest amount in a lifetime, that is, calcium 150mg/(kg·d). ), phosphorus 75mg / (kg · d), full-term children's skin epidermis granule layer also stored 7-dehydrocholesterol, under ultraviolet light, can be converted into vitamin D3, this endogenous vitamin D is only enough after birth 2 ~ 3 months of need, so the amount of vitamin D stored in the newborn depends on the skin development status, when the pregnant woman is heavy during pregnancy or due to partial eclipse, lack of sunshine, pregnancy-induced hypertension syndrome or osteomalacia, as well as twins, premature birth, etc. The reason is that the calcium and phosphorus and/or vitamin D in the newborn are insufficient, so the incidence of neonates in spring and summer in northern China is significantly higher than that in autumn and winter.
Insufficient intake of vitamin D and calcium and phosphorus (15%):
Regardless of the low content of vitamin D in human milk or milk, it is difficult to meet the daily needs of newborns. Human milk contains vitamin D 0-100 U/L, with an average of 22 U/L; milk contains 3-40 U/L, with an average of 14 U/L. Full-term children need to add vitamin D 400U every day. The amount of premature infants needs to be higher, up to 800U/d. However, due to the low intake of milk in premature infants, vitamin D and calcium and phosphorus deficiency are more likely to occur. Human milk contains 340mg/calcium. L, phosphorus 150mg / L, low content, but calcium: phosphorus = 2:1, more suitable for intestinal absorption; milk containing calcium 1200mg / L, phosphorus 900mg / L, calcium: phosphorus = 1.2: 1, not suitable for the intestine The road is absorbed, so the incidence of rickets is higher than that of breast-feeders.
Growth rate is too fast (15%):
The growth rate of bones is directly proportional to the need of calcium and phosphorus. The growth rate of fetuses and newborns in the last 3 months of pregnancy exceeds that of any age group, and vitamin D deficiency is prone to occur.
Insufficient secretion of parathyroid hormone and impaired liver and kidney function (10%):
Insufficient secretion of parathyroid hormone in neonates, renal tubular response to parathyroid hormone is not perfect, resulting in increased reabsorption of phosphorus by the renal tubules and reduced reabsorption of calcium, which may lead to hyperphosphatemia and hypocalcemia in neonates. The calcitonin secreted by magnesium and thyroid C cells is also closely related to vitamin D and calcium and phosphorus metabolism. The impaired liver and kidney function of neonates can also affect the hydroxylation of vitamin D and reduce the biological activity of vitamin D.
Other factors (10%):
The incidence of various diseases in the neonatal period is high, which easily affects the absorption, utilization and metabolism of vitamin D and/or calcium and phosphorus in the liver, gallbladder or kidney, especially the application of ventilator, extra-gastrointestinal nutrient solution to make calcium. Insufficient intake of phosphorus and vitamin D; long-term use of diuretics and sodium bicarbonate to increase urinary calcium excretion; long-term use of anticonvulsant drugs (including pregnant women) such as phenobarbital, stimulate the activation of oxidase system of liver cell microsomes, make vitamins The accelerated decomposition of D3 and 25-(OH)D3 into inactive metabolites can lead to the occurrence of rickets.
Prevention
Neonatal rickets prevention
Prevention of congenital rickets should begin in the second trimester.
1. From the 28th week of pregnancy, give pregnant women vitamin D, 1000U / d, continue to take after the baby is born.
2. Strengthen the health care during pregnancy, pay attention to nutrition, and often carry out outdoor activities to increase the time of daylight exposure.
3. Pregnant women should drink more milk.
4. Actively prevent and cure pregnant women's diseases, such as preventing hepatitis B and protecting kidney function, so as not to affect the metabolism of calcium phosphate and vitamin D in the body. Add vitamin D 50,000 U per month in the third trimester of pregnancy.
5. At present, the prevalence of vitamin D should be increased for newborns, especially premature infants. From the second week after birth, vitamin D can be given to 800-1200 U per day, but it should be noted that the dose of vitamin A should not exceed 10,000 U per day. .
6. Fight for breastfeeding. Human milk contains more calcium and phosphorus and is easy to absorb, especially for infants under 6 months who are competing for breastfeeding.
Complication
Neonatal rickets complications Complications diarrhea neonatal hypocalcemia neonatal seizures children convulsions throat
It is easy to have spontaneous fractures, skeletal deformities such as skull and sternum, and is prone to infectious diseases and diarrhea, forming neonatal hypocalcemia, convulsions or throat, and even death.
Symptom
Symptoms of neonatal rickets common symptoms osteomalacia hypocalcemia sputum closed late beaded rib nodules dyspnea sclerophylla fractures newborns crying baby pillow bald
(A) mental and neurological symptoms : sweating, night terrors, crying, etc., sweating has nothing to do with the climate, due to sweat stimulation, children often rub the occipital, forming occipital baldness or ring hair loss.
(two) osteophyte performance
1. Head.
(1) Skull softening: It is an early manifestation of rickets, which is more common in infants from March to June.
(2) Cranial deformity: "square skull", "saddle head" or "crosshead"
(3) The front is large, the closure is late, and it can be closed until 2-3 years old.
(4) Late teething can be extended to 1 year old teething, or 3 years old, and the teeth are not aligned and the enamel is poorly developed.
2. Chest.
(1) The ribs are affected by beads.
(2) Thoracic deformity: chicken chest; funnel chest.
3. Limbs and spine.
(1) The wrist and ankle are inflated to form a bangle and a foot bracelet.
(2) Lower limb deformity "O" shaped leg (knee varus), or "X" shaped leg (knee valgus).
(3) curvature of the spine: there may be scoliosis or kyphosis. In severe cases, pelvic deformity (hip valgus) may also be seen. In severe cases, women may become dystocia due to pelvic deformity in adulthood.
(3) Other performances : look up, sit, stand, walk late, joints are loose and overextended, cerebral cortical function is abnormal, conditioned reflex formation is slow, language development is backward, anemia.
Examine
Neonatal rickets
1. Laboratory inspection:
(1) Alkaline phosphatase appears earlier in the course of rickets, and recovery is the latest, which is conducive to examination and diagnosis.
(2) Determination of serum 25(OH)D3 or 1,25(OH)2D3 levels, the value of which is zero in typical rickets, and also significantly decreased in subclinical rickets, and vitamin D can be significantly increased after treatment, which is sensitive. Reliable biochemical indicators.
2, X-ray inspection:
The diagnosis of neonatal rickets relies heavily on X-ray examination. X-ray changes in typical infantile rickets can also be seen in the neonatal period, such as loose bones, reduced bone density, sparse trabecular bone, and cortical bone. Thinning and thinning of the calvaria; the long bones are widened, the temporary calcification is blurred, widened, and the edges are cloud-like or brush-like, and there is a cup-shaped depression, and the nucleus is blurred, and the nucleus is ambiguous. Widening of the end distance, usually in the chest X-ray film, accidentally found in the rib costal cartilage junction similar to the long bones of the rickets, sometimes spontaneous fractures, distal femur or proximal humerus When the bone nucleus is not present, congenital rickets should be considered. The X-ray findings can be divided into three phases:
1. Initial stage: the ulnar metaphysis is blurred, the cortical bone density is slightly reduced, and the humerus changes slightly or unchanged.
2. Stimulating period I: The ulnar metaphysis is blurred, the rough is more obvious, the density is reduced, the metaphysis of the humerus is blurred, and the density is reduced.
3. Inflammatory phase II: The ulnar humerus is obscure, rough, temporary calcification disappears, and bone density is significantly reduced.
Diagnosis
Diagnosis and diagnosis of neonatal hysteria
Diagnose based on:
1. History: The cause of rickets can be investigated, especially the history and performance of vitamin D and calcium and phosphorus deficiency in pregnant mothers.
2. Clinical manifestations: have certain clinical manifestations, such as hyperhidrosis and low-calcium throat; bone changes, such as skull softening, skull, sternum and other skeletal deformities, or spontaneous fractures.
3. The X-ray of the bone changes.
4. Blood biochemical changes.
5. Bone Density Detection: In recent years, the detection method of bone density by ultrasound has been established, and it is expected to replace the monitoring of X-ray.
Differential diagnosis
When neonatal rickets develop hypocalcemia, it should be differentiated from hypothyroidism; when anterior sputum enlargement, cranial suture widening, head circumference enlargement and other deformities should be differentiated from hydrocephalus; neonatal rickets should be Identification with anti-vitamin D rickets, cartilage dystrophy, dependence on vitamin D and/or calcium deficiency, laboratory and auxiliary examination, and treatment with vitamin D preparations can help identify.
