Physiological jaundice of neonates
Introduction
Introduction to neonatal physiological jaundice Neonatal physiological jaundice is caused by the characteristics of neonatal bilirubin metabolism and is a physiological phenomenon in the growth of normal newborns. Astragalus membranaceus is caused by yellowing of skin, mucous membranes or other organs due to the increase of bilirubin in the body. When adult serum bilirubin is >34mol/L (2mg/dl), yellow staining can be seen on the sclera and skin, and neonates are due to capillaries. When the bilirubin is >85mol/L (5mg/dl), skin yellowing occurs. basic knowledge Sickness ratio: 5% Susceptible people: children Mode of infection: non-infectious Complications: neonatal bilirubin encephalopathy
Cause
Neonatal physiological jaundice
More bilirubin production (25%):
There are many reasons for bilirubin production:
(1) Red blood cell destruction: The fetus is in a hypoxic environment in the uterus, and the red blood cells are compensatory, but the life span is short, the blood oxygen content is increased after birth, and too many red blood cells are rapidly destroyed.
(2) There are many sources of bypass bilirubin.
(3) high heme oxygenase content: high content within 7 days after birth, the potential for producing bilirubin is large.
Liver function is immature (30%):
(1) Poor ability of liver to take bilirubin: Insufficient content of Y and Z protein in liver cells, so that the liver does not take up enough bilirubin.
(2) Poor liver-binding bilirubin function: low intraglycemia glucuronyltransferase activity and insufficient viability, resulting in poor function of binding bilirubin.
(3) poor function of liver excretion bilirubin: poor function of excretion combined with bilirubin, easy to cause cholestasis.
Intestinal-hepatic circulation factors (30%):
When the newborn is born, the normal flora in the intestine has not been established, and the bilirubin entering the intestinal tract cannot be converted into urobilinogen (fecal biliary tract), and the -glucuronidase activity in the intestinal tract of the newborn is high. The bound bilirubin in the intestine is hydrolyzed to glucuronic acid and unbound bilirubin, which in turn is absorbed by the intestinal wall through the portal vein to the liver.
Due to the above characteristics, the ability of newborns to ingest, combine, and excrete bilirubin is obviously less than that of adults, and bilirubin is produced more and excreted less. Therefore, jaundice is highly prone to occur, especially in hypoxia, delayed meconium discharge, and delayed feeding. Vomiting, dehydration, acidosis, head hematoma, etc. will aggravate jaundice.
Pathogenesis
The occurrence of physiological jaundice is related to the characteristics of neonatal bilirubin metabolism.
1. More bilirubin production: Newborns produce more than twice as much bilirubin (8.5 mg/kg) per day than adults (3.8 mg/kg).
2. Insufficient delivery of blood protein linkage: Newborns have more or less acidosis after birth, so it often shows insufficient connection between bilirubin and albumin, especially albumin levels in premature infants are low, such as improper medication, medical source The substance that competes for albumin is sexually added, and the transport of bilirubin is blocked.
3. Liver-dirty treatment of bilirubin is poor: such as liver uptake, transformation, lack of ability to excrete bilirubin, a series of enzymes in the process of intrahepatic bilirubin and glucuronic acid need energy and oxygen, If the newborn is born, postpartum hypoxia, cold damage, acidosis, and toxins produced during infection, the enzyme function is inhibited, especially the important role of glucuronyltransferase in the liver of newborn newborns. The content is very low, resulting in poor handling of bilirubin.
4. The liver-intestinal circulation load is large: due to the action of glucosidase in the neonatal intestine, the binding of bilirubin to unconjugated bilirubin is reabsorbed in the intestinal lumen, and the newborn forms about 20 mg of bilirubin every day. If the meconium discharge is delayed, the hepatic-intestinal circulation load of bilirubin increases.
Prevention
Neonatal physiological jaundice prevention
Physiological jaundice prevention method
1. Experts remind that if a woman has had a baby with fetal yellow, she should be prevented from pregnancy and take Chinese medicine on time.
2, after the baby is born should closely observe heart rate, heart sounds, anemia and liver size changes, early prevention and treatment of heart failure.
3, the baby is closely observed after the birth of the sclera jaundice, found that jaundice should be treated as soon as possible, and observe the change of jaundice color to understand the advance and retreat of jaundice.
4. If you need to carry out blood transfusion therapy, you should do a good job of air disinfection in the hospital room, prepare blood and various medicines and articles, and strictly operate the procedures.
5, prevention of neonatal jaundice should pay attention to protect the baby's skin, umbilicus and buttocks to prevent damage.
6, pay attention to observe the systemic symptoms of fetal yellow baby, with or without mental wilting, lethargy, difficulty in breast-feeding, convulsions, strabismus, limbs, or convulsions, so as to treat the severely ill children early.
7, fetal yellow often suffer from damp heat in the pregnant mother and affect the fetus, resulting in fetal fetal yellow after birth, so during pregnancy, pregnant mothers should pay attention to diet, but eat cold, but hungry, and avoid alcohol and hot The product to prevent damage to the spleen and stomach.
Complication
Neonatal physiological jaundice complications Complications neonatal bilirubin encephalopathy
The vast majority have no complications, and some very low birth weight children may develop bilirubin encephalopathy.
Symptom
Neonatal physiological jaundice symptoms Common symptoms Baby face yellowish skin yellow sclera yellow stained jaundice
1. Physiological jaundice is light yellow limited to the face and neck, or affects the trunk, the sclera can also be yellow-stained, subsided after 2 to 3 days, and the skin color returned to normal on the 5th to 6th. Severe jaundice can also be used throughout the body, vomit and cerebrospinal fluid can also be yellow-stained for more than 1 week, especially for individual premature babies lasting for 4 weeks, the feces are still yellow, no bilirubin in urine Prime.
2. The color of the yellow scorpion is light, the color is darker, but the skin is rosy and the yellow is red.
3. The jaundice is more common in the trunk, the sclera and the proximal extremities, but the elbow and knee.
4. The general condition of the newborn is good, no anemia, no swelling of the liver and spleen, normal liver function, no nuclear jaundice.
5. Physiological jaundice in premature infants is more common than that in full-term children. It can be delayed by 1 to 2 days. The degree of jaundice is heavier and the regression is delayed. It can be extended to 2 to 4 weeks.
Examine
Examination of neonatal physiological jaundice
1. Serum bilirubin, multiple measurements gradually increase suggesting biliary atresia, if there is fluctuation or irregular decline, suggesting hepatitis.
2. Serum transaminase, a significant increase in early is a hint of hepatitis.
3. Other laboratory tests, serum 5'-nucleotidase significantly increased suggestive of biliary atresia. Serum alpha-fetoprotein >40 mg/L suggests hepatitis. Duodenal drainage fluid containing bile or bile acid can reduce external biliary atresia. Lipoprotein-X (LP-X) positive patients suggest biliary atresia.
4. Intravenous injection of 131I rose red 37 ~ 148MBq (1 ~ 4Ci), collect 3 days of feces (can not be mixed with urine) to measure counts per minute, such as > 10% of the injection can eliminate biliary atresia.
5. Radionuclide liver and biliary scan were performed after 99m labeled iminodiacetic acid (IDA) derivative. The liver development of children with hepatitis was slow and the intestinal tract showed radioactive concentration. The liver development of children with biliary atresia appeared quickly. No development in the intestines.
6. B ultrasound, can be found in the total biliary tract cyst, such as no gallbladder suggestive biliary atresia.
7. Liver biopsy, liver structure is basically normal, massive hyperplasia of bile ducts suggest biliary atresia. Hepatic lobular structure disorder, hepatocyte necrosis, multinucleated giant cells are easy to see suggestive of hepatitis.
8. Exploratory laparotomy, strive to be implemented within 2 months, if no gallbladder should be further explored. If there is gallbladder, gallbladder angiography should be performed. If abnormal, hepatic jejunostomy should be performed (the sooner the effect is performed, the latest is not more than 3 months).
Diagnosis
Diagnosis and identification of neonatal physiological jaundice
diagnosis
(1) medical history
1. The appearance time of jaundice, the common sputum within 24 hours should first consider neonatal hemolysis, and then consider congenital infections such as CMV. Physiological jaundice is most common in 2 to 3 days, and ABO is also excluded. 4 to 7 days are more common with sepsis and breast milk jaundice. Seven days later, jaundice, sepsis, neonatal pneumonia, biliary atresia, and breast milk jaundice were all possible.
2. Astragalus develops rapidly, neonatal hemolysis is the fastest, followed by sepsis, neonatal hepatitis and biliary atresia develop slowly and lasting.
3. The color of feces and urine, the color of the feces is very light or gray, and the urine color is deep, suggesting neonatal hepatitis or biliary atresia.
4. Family history, patients with faba bean disease should consider whether G6PD deficiency disease, parents should have hepatitis.
5. Pregnancy history, production history (premature rupture of membranes, prolonged labor, suggesting birth-time infection), history of medication used by mother before labor.
(B) the stool has obvious pigments should consider neonatal hemolysis and sepsis
1. If there is infection and poisoning, blood and urine culture should be carried out.
2. If there is hemolysis (reticulocyte growth, nucleated red blood cells > 2 ~ 10/100 white blood cells), the mother and baby ABO and Rh blood type should be checked, and the anti-human globulin test positive is Rh blood type incompatibility. The antibody release test was positive in children with ABO hemolytic disease. Those who are negative in the above test or those who develop after 3 or 4 days of birth should be excluded from the G6PD defect.
Differential diagnosis
Identification with pathological jaundice, pay attention to observe the time and evolution of jaundice, such as the appearance of jaundice, appeared within 24h after birth. Huang Qi disappeared late and continued to retreat. Or reappear after the physiological jaundice subsides. Or jaundice continued to increase, etc., all of which are pathological jaundice, clinically associated with abnormal symptoms and signs of jaundice, are pathological jaundice, pathological jaundice can cause bilirubin encephalopathy, should actively identify the cause, actively yellow treatment.
