1、第二節 新生兒黃疸（Second neonatal jaundice）Second neonatal jaundiceJaundice is a common clinical symptom in the neonatal period. Serum bilirubin levels in normal subjects ranged from 3.4 to 13.7 Mu mol /L (0.2 to 0.8mg/dl), and over 25.7 to 34.2 mu mol/L (1.5 to 2.0mg/dl), indicating jaundice. But the newbo

2、rn skin blood vessel is rich, the color rosy, the serum bilirubin content reaches 51.3 68.4 mu mol/L (3 4mg/dl), the naked eye can distinguish jaundice. Jaundice in older children or adults is a pathological phenomenon, and the newborn is divided into two physiological and pathological types. Any on

3、e of the following cases of neonatal jaundice, should be regarded as pathological jaundice of premature infants: jaundice in 24 hours after birth, premature jaundice within 48 hours; the jaundice is heavy: serum bilirubin more than normal children of the same age average, or per day increased by mor

4、e than 85.5 mol/L (5mg/dl); the duration of jaundice is too long (more than 2 weeks or more full-term infants, preterm infants more than 3 weeks), or the reappearance of back jaundice; jaundice associated with other clinical symptoms, or serum bilirubin more than 25.7 mol/L (1.5mg/dl).First, the cha

5、racteristics of neonatal bilirubin metabolismThe occurrence of physiological jaundice in neonates is related to the metabolism of bilirubin in newborns.(a) bilirubin relatively excessive fetal intrauterine hypoxia in the living environment, the number of red blood cells is relatively more, if you we

6、re born when delayed umbilical cord ligation or midwives intends to squeeze blood from the umbilical cord to the newborn is more, the number of red blood cells. Fetal red blood cell life is short (70100 days), so the quantity that produces bilirubin is much also. After birth, the lung began to breat

7、he, and the partial pressure of oxygen increased. Excessive red blood cells rapidly destroyed and increased unconjugated bilirubin in the blood. Adults produce about 65 mol/L (3.8mg/kg) of bilirubin per day, and the newborn produces about 145.4 mol/L (8.5mg/kg) of bilirubin per day, equivalent to 2

8、times that of adults, so the burden of bilirubin metabolism in the newborn liver is greater than that in adults.(two) the ability of bilirubin and albumin to transport is insufficient; the transient stage of neonatal birth is characterized by acid poisoning, which affects the amount of bilirubin and

9、 albumin. The albumin in the blood of the premature infants is on the low side, which leads to the delay of the coupling of bilirubin.(three) the ability of liver cells to absorb unconjugated bilirubin is poor, and the lack of Y protein and Z protein in adult hepatocytes (only 5 to 20% in adults) is

10、 gradually synthesized at fifth days after birth. These two proteins have the function of uptake of unconjugated bilirubin and transport to the smooth endoplasmic reticulum. The lack of synthesis of Y and Z proteins affects the uptake of unconjugated bilirubin by hepatocytes.(four) glucuronic acid l

11、iver system immature neonatal liver transferase and uridine phosphate dehydrogenase two (UDPG dehydrogenase deficiency) or inhibited, not unconjugated bilirubin into conjugated bilirubin and unconjugated bilirubin in the blood and hair retention jaundice. These enzymes begin to increase only about 1

12、 weeks after birth, and preterm babies are later.(five) the enterohepatic circulation of the newborns the first few days of life, the normal intestinal flora has not yet been established, so with the unconjugated bile into the intestines cannot be reduced to stercobilin yuan; on the other hand, the

13、neonatal intestine had more beta glucuronidase, can be hydrolyzed to unconjugated bilirubin bilirubin, which is intestinal mucosal absorption, return to the liver via the portal vein, which is a characteristic of neonatal intestinal hepatic circulation. As a result, the burden of bilirubin on the li

14、ver is increased, resulting in unconjugated bilirubin retention in the blood.Two, physiological jaundiceMost newborns have yellow skin and / or mucous membranes on the 23 day after birth. They are in good general condition, and have no other pathological conditions. The patients who have gone down f

15、or about one week are called physiologic jaundice.(I) clinical manifestationMost of the physiological jaundice in 23 days after birth, fourth to 6 days of the most obvious, the majority of full-term babies in 710 days after the birth of extinction, premature infants can be delayed to third to 4 week

16、s subsided.Jaundice first in the face, neck, and then can spread throughout the trunk and limbs, generally a little yellow, sclera may be slightly yellow, but the soles of the hands are not yellow. In addition to jaundice,Children in general health, good, without other clinical symptoms, stool color

17、 is normal.(two) laboratory examinationUmbilical cord blood bilirubin in normal neonates up to about 51.3 mol/L (3mg/dl), born in about 4 days after the peak, generally not more than 171 205 mol/L (10 12mg/dl), preterm infants less than 256.5 mol/L (15mg/dl), then gradually restore. VDB is indirect

18、reaction. Bilirubin in urine is negative and fecal pigment is increased.(three) the common causes and treatment of delayed extinctionThe causes of physiological jaundice are manifold and comprehensive, so the severity and extinction time are often influenced by the following factors.1. mothers prena

19、tal medication: such as mothers prenatal use of a large number of oxytocin or vitamin K and so on.Asphyxia and hypoxia occur during the 2. stage of labor. As a result of dyspnea and hypoxia, on the one hand it aggravates acidosis, on the other hand, it inhibits the activity of glucuronic acid transf

20、erase and affects the metabolism of bilirubin;3. bleeding during childbirth causes increased bilirubin production;4. postpartum cold and hunger: the body of free fatty acid and other organic anions increased, combined with bilirubin and albumin and bilirubin competition, free blood, delayed feeding,

21、 delayed passage of meconium, can increase intestinal hepatic circulation, increase blood bilirubin to non binding.In order to prevent the occurrence of hyperbilirubinemia of newborn, maternal prenatal medication should be careful, do not try to do drug delivery; in the course of intensive care, in

22、order to avoid the occurrence of fetal asphyxia and birth injury after birth; keep the neonatal body temperature, appropriate early feeding. If neonatal hyperbilirubinemia occurs, except for etiological treatment, phototherapy, plasma or albumin therapy can be used.Three, neonatal hepatitisAs the on

23、set in neonatal period a group of clinical syndrome, mainly for obstructive jaundice, hepatomegaly and liver function damage, because the etiology, the exact cause of each case is difficult to determine, it is often referred to as neonatal hepatitis syndrome (Neonatal Hepatitis Syndrome).(1) cause o

24、f diseaseMainly caused by viruses, such as hepatitis B virus, cytomegalovirus, rubella virus, herpes simplex virus and enterovirus. Toxoplasmosis, protozoa, Li Si, syphilis, and so on, are also the cause of the disease.(two) clinical characteristicsOnset is slow. Jaundice usually occurs within days

25、to days after birth, and has a long duration. It can be accompanied by anorexia, nausea, vomiting, indigestion, and loss of weight. Stool color becomes pale, severe can be gray, but sometimes shallow, deep dynamic changes. Deep yellow urine color. The liver is mild to moderately enlarged and slightl

26、y rigid. A small number of spleens are also large. Toxic hepatitis often has infection focus and systemic poisoning symptoms. Rubella virus, cytomegalovirus hepatitis, often associated with congenital malformations or intrauterine growth disorders.Laboratory examination of serum transaminase increas

27、ed, bilirubin increased, combined bilirubin increased mainly, flocculation turbidity test early change was not obvious. Alpha fetoprotein positive. Uric bile element is positive, uric bilirubin can be positive or negative according to obstruction of bile duct. Blood sampling examination of hepatitis

28、 B virus surface antigen, collection of baby urine or cervical scraping film, looking for giant cell inclusion body, etc., can be etiological diagnosis.(three) treatment;To protect liver treatment mainly, provide sufficient heat and vitamins. Disable drugs that are toxic to the liver. Jaundice sever

29、e, can use prednisone (2mg/kg/ days) anti-inflammatory, to alleviate bile duct obstruction, usually 48 weeks, should pay attention to the prevention of other infections. The general case used traditional Chinese medicine heat dampness Tuihuang soup, like Chen hao. Cause clear, for the treatment of t

30、he cause.Four congenital biliary atresia(1) cause of diseaseUnknown etiology. It is generally considered to be related to intrauterine viral infection, secondary hepatic duct inflammation, secondary obstruction, and congenital biliary tract malformation. The intrahepatic bile duct, hepatic duct or c

31、ommon bile duct may develop atresia or agenesis, and the gallbladder may also develop atresia or dysplasia.(two) clinical characteristicsJaundice usually occurs 13 weeks after birth and continues to subside,Progressive exacerbation. Meconium can be blackish green, but soon after birth it will turn w

32、hite. In severe cases, the appearance of gray stools is pale yellow due to the infiltration of bilirubin by intestinal epithelial cells. Progressive enlargement of the liver, gradually hardened. The majority had splenomegaly, ascites occurred late. Early children well appetite, nutritional status mo

33、stly are good; late because of fat and fat soluble vitamin malabsorption, nature gradually weak, can be made of vitamin A, D, K deficiency caused by dry eye, rickets and bleeding tendency.Laboratory examination showed that serum bound bilirubin and alkaline phosphatase increased continuously. Early

34、liver function is normal, advanced period has unusual change. Positive urine bilirubin, urine bile negative. Have to do 99m IDA radionuclide technetium - (acetyl-p-aniline imine two acetic acid) imaging, intravenous injection of tracer within 6 hours, the intestinal tract does not appear to support

35、the diagnosis of radioactive concentration.(three) treatment;Congenital biliary atresia should be treated within 3 months after birth. At present, the highest success rate is liver hilum jejunum anastomosis. However, the possibility and effect of operation vary depending on the type of deformity, an

36、d the operation is difficult for patients with hepatic obstruction.Five. Hemolytic disease of the newbornHemolytic diseaseof newborn (hemolytic disease of the newborn) is due to maternal and infant blood group incompatibility caused by the same immune hemolysis. In our country, the majority of ABO b

37、lood group incompatibility, less Rh blood group, the other such as MN, Kell blood group system is rare.(1) cause of diseaseWhen the fetus and mother of paternal antigens by genetic gains into the mother is not at the same time, after will stimulate the mother to produce antibodies, can enter the fet

38、us through the placenta, antigen antibody reaction leads to hemolysis and fetal red blood cells.In the ABO system, because the O type person has the anti A or the anti BigG number to be more than the A type and the B type: A antigen is stronger than B antigen's antigenicity, therefore mother O t

39、ype, fetal A type person has the opportunity to be many. ABO hemolytic disease can occur in the first fetus, and the mother has been stimulated by antigens similar to A and B in nature, which have been associated with anti A or anti B antibodies. Rh hemolytic immune antibodies, can only be stimulate

40、d by human blood cells as antigen, and if the fetus in the delivery of fetal red blood cells into the mother, in addition to the history of blood transfusion, rare, the first fetus that is the incidence. Most people in China are Rh positive, so Rh hemolytic disease is rare in our country.(two) clini

41、cal manifestationThe weight of this disease symptom is very big, the symptom of general ABO blood group is opposite, Rh blood group is opposite the person is light. Children often after birth in 24 hours or second days of jaundice, and increase rapidly. With the deepening jaundice may appear severe

42、anemia, hepatosplenomegaly, bilirubin encephalopathy. Rh is incompatible with a large number of hemolytic agents. It has serious anemia at birth. It can lead to heart failure, systemic edema, or even stillbirth.(three) diagnosisAccording to the clinical features of jaundice and hemolytic anemia afte

43、r 24 hours, combined with the identification of mother and infant blood group and specific antibody examination, the diagnosis can be made definitely. Serological examination items and their clinical significance are shown in table 2-3.Table 2-3 serological examination items and clinical significanc

44、e of hemolytic disease of the newbornBlood type neonatal serology test; maternal serology examination; clinical significanceDirect maternal and child resistanceGlobulin test indirect resistanceGlobin test; release test; free antibodyinspectO A modified method + release of IgG, anti A, IgG, anti A+,

45、ABO hemolytic disease (anti A)O B modified method + release of IgG, anti B, IgG, anti B+, ABO hemolytic disease (anti B)Rh- Rh+ + anti D antibody +Anti E antibody +Anti C antibody + anti D incomplete antibodyAnti E, incomplete antibodyThere are anti C, incomplete antibodies, Rh hemolytic disease (an

46、ti D)Rh hemolytic disease (anti E)Rh hemolytic disease (anti C)(four) treatment;Comprehensive measures should be taken to reduce serum bilirubin concentration and correct anemia according to the severity of the disease. General use of drugs and phototherapy, and when necessary, exchange transfusion.

47、1. drug therapyThe main objective is to reduce serum unconjugated bilirubin and prevent bilirubin encephalopathy. Combination of Chinese and Western medicine.The Western Medicine(IV) albumin, which is supplied by plasma or albumin, is associated with bilirubin, which reduces the free unconjugated bi

48、lirubin and prevents bilirubin encephalopathy. Plasma 25ml/ times intravenous injection (100ml plasma containing albumin, 3G, 1g albumin can bind unconjugated bilirubin 8.5mg) or albumin lg/kg plus 25% glucose, 10 20ml intravenous drip, 12 times a day.The lack of some content - here. ".5g, Rhiz

49、oma Coptidis, 1.5g, rhubarb, 3G. The YCHT Artemisia 1.5g, gardenia 9g, rhubarb 3G, licorice 1.5g. The Xiaohuang Lidan Granule Artemisia 9g, gardenia 3G, rhubarb 3G, couchgrass root 10g, Desmodium 6G, Poria 6g.The above three parties may choose one of them, take 1 doses daily, and take them before me

50、als. There are also intravenous drug users, whose efficacy is faster than oral administration.2. phototherapyThe principle of bilirubin can absorb light phototherapy, in light and oxygen under the effect of fat soluble bilirubin oxidation has become a kind of water soluble products (light oxidation

51、of bilirubin, namely Dipyrrole), can be excreted from bile or urine, thereby reducing serum unconjugated bilirubin concentration. Absorption band is 400 500 nm of bilirubin, especially in the 420 440 nm wavelength time decomposition was the strongest, blue fluorescence peak wavelength is between 425

52、 to 475 nm, so the blue fluorescent lamp treatment. In recent years, green light has been reported to be more effective than blue light.The phototherapy methods and precautions to let children naked sleep in the blue light from the light source box central, infantile 50cm, eyes and genitals with bla

53、ck or black cloth cover cover. The chamber temperature should be kept at 3032 degrees centigrade, and the anus temperature was measured 1 times per hour, keeping the body temperature between 36.5 and 37.2 degrees centigrade. The time of illumination was determined according to the cause of disease,

54、the severity of the disease and the decrease of serum bilirubin concentration. It could be irradiated for 2472 hours continuously.Phototherapy has a weak effect on conjugated bilirubin. When the serum bilirubin >64.8 mol/l (4mg/dl), transaminase and elevated alkaline phosphatase, phototherapy aft

55、er biliverdin accumulation, can make the skin a bronze, namely the bronze disease. The combination of bilirubin or liver function damage in children for phototherapy.3. exchange transfusionThe purpose for exchange transfusion sensitized red cell and antibody has caused bleeding, prevent further hemo

56、lysis; reduce the serum unconjugated bilirubin concentration, the prevention of bilirubin encephalopathy; correction of anemia, prevent heart failure.The blood transfusion indications of prenatal diagnosis of hemolytic disease of the newborn is born, anemia, edema, hepatosplenomegaly and heart failu

57、re, blood hemoglobin < 120g/L. The umbilical cord blood bilirubin > 59.84 68.4 mol/L (3.5 4mg/dl), or 6 hours after birth to 102.6 mol/L (6mg/dl), 205.2 mol/l (13mg/dl) 12 hours after birth; the bilirubin has reached 307.8 342 mol/L (18 20mg/dl) and bilirubin in preterm infants up to 273.6 mol

58、/L (16mg/dl) 4; there are early symptoms of bilirubin encephalopathy.The serum ABO hemolytic disease with AB plus O hybrid plasma, red blood cell blood. Rh hemolysis should be ABO isotype (or type O) and Rh negative heparin blood. Blood sources should be fresh blood within 3 days.The change of blood volume and blood transfusion speed commonly used amount is 85ml/kg, about 2 times the infant blood. The amount of blood extracted and injected each time is 10 20ml, the condition is hea