《2018 昆士兰产科与新生儿临床指南：新生儿黄疸》 重点内容(全文)

浅谈新生儿黄疸王惠霞发表时间：2018-11-19T15:43:29.280Z 来源：《航空军医》2018年16期作者：王惠霞[导读] 医学上把未满月（出生28天内）新生儿的黄疸，称之为新生儿黄疸（neonatal jaundice），新生儿黄疸是指新生儿时期。

（宁夏第五人民医院石炭井医院九竹社区卫生服务站）概述：医学上把未满月（出生28天内）新生儿的黄疸，称之为新生儿黄疸（neonatal jaundice），新生儿黄疸是指新生儿时期，由于胆红素代谢异常，引起血中胆红素水平升高，而出现以皮肤、黏膜及巩膜黄染为特征的病症，是新生儿中最常见的临床问题。

本病有生理性和病理性之分。

生理性黄疸是指单纯因胆红素代谢特点引起的暂时性黄疸，在出生后2～3天出现，4～6天达到高峰，7～10天消退，早产儿持续时间较长，除有轻微食欲不振外，无其他临床症状。

若生后24小时即出现黄疸，每日血清胆红素升高超过5mg/dl或每小时＞0.5mg/dl；持续时间长，足月儿＞2周，早产儿＞4周仍不退，甚至继续加深加重或消退后重复出现或生后一周至数周内才开始出现黄疸，均为病理性黄疸。

一．病因1.生理性黄疸的病因1）与新生儿胆红素代谢特点有关，包括胆红素生成相对较多；2）肝细胞对胆红素的摄取能力不足；3）血浆白蛋白联结胆红素的能力差；胆红素排泄能力缺陷；肠肝循环增加。

因此60%足月儿和80%早产儿在生后第1周可出现肉眼可见的黄疸。

2.病理性黄疸病因1）胆红素生成过多因过多的红细胞的破坏及肠肝循环增加，使血清未结合胆红素升高。

常见的病因有：红细胞增多症、血管外溶血、同族免疫性溶血、感染、肠肝循环增加、红细胞酶缺陷、红细胞形态异常、血红蛋白病、维生素E缺乏和低锌血症等。

2）肝脏胆红素代谢障碍由于肝细胞摄取和结合胆红素的功能低下，使血清未结合胆红素升高。

常见的病因有：缺氧和感染、Crigler-Najjar综合征（先天性尿苷二磷酸葡萄糖醛酸基转移酶缺乏）、Gilbert综合征（先天性非溶血性未结合胆红素增高症）、Lucey-Driscoll综合征（家族性暂时性新生儿黄疸）、药物（如磺胺、水杨酸盐、吲哚美辛、毛花苷丙等）、先天性甲状腺功能低下、垂体功能低下、21-三体综合征等。

新生儿黄疸，这些内容你可能不知道!发布时间：2021-05-26T08:03:40.648Z 来源：《健康世界》2021年3期作者：黄秋华[导读] 对于每一个即将来到世界上的宝宝，我们都希望她/他可以健康平安的降临，但是这其中却有不少宝宝刚刚落地就被一个健康问题所困扰，它就是新生儿黄疸。

我想对于新生儿黄疸大多数家长都不会感到陌生，这是一种新生儿常见疾病，据相关调查数据显示，在足月儿中，新生儿黄疸的发病率为60%，而早产儿的发病率则高达80%以上。

黄秋华中江县妇幼保健院四川德阳 618100对于每一个即将来到世界上的宝宝，我们都希望她/他可以健康平安的降临，但是这其中却有不少宝宝刚刚落地就被一个健康问题所困扰，它就是新生儿黄疸。

我想对于新生儿黄疸大多数家长都不会感到陌生，这是一种新生儿常见疾病，据相关调查数据显示，在足月儿中，新生儿黄疸的发病率为60%，而早产儿的发病率则高达80%以上。

虽说新生儿黄疸很常见，但是对于家长来讲，宝宝刚来到自己怀里没几天就要被送到暖箱中治疗，这是很难接受的一件事情。

还有一些父母对此会感到困惑，为什么同为新生儿黄疸，有些宝宝需要治疗，而有些宝宝不需要治疗呢？本文就是来为各位宝爸宝妈们解答疑惑的，下面就新生儿黄疸问题作者想和大家好好说道说道。

一、新生儿黄疸是什么？新生儿黄疸指的是新生儿时期，因胆红素代谢异常以致于血液中胆红素水平升高，从而诱发皮肤、黏膜、巩膜等部位出现以黄染为主要特征的疾病，该病是新生儿常见的临床问题之一，新生儿患病后可出现皮肤暗沉无光泽、便秘、心律不齐以及腹部肿胀等表现。

其实在我们每个人的血液中都含有少量的胆红素，但是与成年人相比，新生儿体内红细胞数量更多一些，寿命更短一些，再加上血红蛋白半衰期短等因素，则会造成新生儿体内胆红素生产过多的发生，另外，新生儿在出生以后即可拥有自主呼吸，并不需要大量的红细胞搬运氧气，而这些被破坏掉的红细胞则会释放血红素，最终被分解成为胆红素。

黄疸预防及治疗指南黄疸，又称黄疸病，是一种常见的疾病，特征是皮肤和黏膜出现黄色。

黄疸通常是由于胆红素在体内积累过多而引起的，而胆红素的积累则可能是由于肝脏功能异常、胆道阻塞或红细胞破坏过多等原因引起的。

黄疸的预防和治疗至关重要，下面将为大家介绍黄疸的预防和治疗指南。

黄疸的预防是非常重要的，尤其是对于新生儿来说。

新生儿黄疸是一种常见的疾病，主要是由于新生儿肝脏功能不完善导致胆红素无法正常代谢。

为了预防新生儿黄疸，以下几点是非常重要的：首先，母乳喂养是预防新生儿黄疸的重要措施之一。

母乳中含有丰富的酶和盐酸，可以促进胆红素的代谢和排泄，减少胆红素在体内的积累。

因此，建议新生儿尽早进行母乳喂养，并保证充足的母乳摄入量。

其次，控制新生儿的光照时间也是预防黄疸的重要措施。

光照可以促进皮肤中胆红素的转化和排泄，减少胆红素在体内的积累。

因此，建议新生儿每天进行适量的户外活动，增加阳光照射时间。

此外，新生儿黄疸的预防还包括定期进行体检和监测胆红素水平。

定期的体检可以及时发现新生儿黄疸的症状，及早采取措施。

监测胆红素水平可以帮助医生评估新生儿的黄疸程度，从而制定相应的治疗方案。

对于已经发生了黄疸的患者，及时的治疗也是非常重要的。

黄疸的治疗主要包括以下几个方面：首先，针对黄疸的原因进行治疗。

黄疸的原因可能是多种多样的，如肝脏功能异常、胆道阻塞等。

因此，在治疗黄疸时，首先需要明确黄疸的原因，并针对原因进行相应的治疗。

其次，对于黄疸患者来说，保持良好的生活习惯也是非常重要的。

合理的饮食结构和规律的作息时间可以帮助身体恢复正常功能，促进胆红素的代谢和排泄。

此外，黄疸患者还可以适当进行一些辅助治疗，如草药疗法、中医针灸等。

这些辅助治疗可以帮助患者缓解黄疸的症状，促进身体的康复。

总之，黄疸的预防和治疗是非常重要的，尤其是对于新生儿来说。

通过合理的预防措施和及时的治疗，可以有效地预防和治疗黄疸，减少其对身体的损害。

希望以上介绍的黄疸预防和治疗指南能对大家有所帮助。

新生儿黄疸健康教育资料(含基本知识、治疗方案、预防措施)新生儿黄疸是新生儿时期常见情况之一，是儿科医生每天都会遇到的问题。

大部分健康新生儿出生后可有暂时性高胆红素血症称为“生理性黄疸”，但也只有在新生儿期因血清胆红素浓度的增高特别是高未结合胆红素血症可直接威胁新生儿的生命，或造成严重的中枢神经系统后遗症，因此需要对新生儿黄疸引起足够重视。

1基本知识新生儿黄疸分为生理性和病理性黄疸。

生理性黄疸原因主要与新生儿胆红素代谢特点有关。

常因红细胞破坏过多导致肝细胞胆红素负荷增加、肝细胞摄取、结合、排泄胆红素的功能不足、新生儿肠腔内β-葡萄糖酸苷酶在pH偏碱情况下使结合胆红素分解重新变成未结合胆红素而通过肠道吸收进入血循环等因素出现黄疸。

尤其是在饥饿、缺氧、酸中毒、脱水、胎粪排出延迟、溶血性疾病颅内出血、等情况时黄疸加重。

生理性黄疸：由于新生儿胆红素代谢特点，约50-60%足月儿和80%以上早产儿于生后2-3天出现黄疸，4-5天达到高峰，足月儿在生后10-14天消退，早产儿在生后3-4周消退。

血清胆红素峰值足月儿不超过12.9mg/dl，早产儿不超过15mg/dl。

在黄疸出现期间新生儿一般情况良好。

病理性黄疸：有以下特点：1、黄疸于出生后24小时之内出现。

2、黄疸程度重，血清胆红素值，足月儿＞12.9 mg/dl ，早产儿＞15mg/dl。

3、血清胆红素值上升速度快，超过5 mg/dl。

4、直接胆红素＞2 mg/dl。

5、黄疸持续时间延长：足月儿＞3周，早产儿＞4周。

6、黄疸退而复现，即黄疸在新生儿生理性黄疸消退后再次出现。

引起病理性黄疸病因很多，常见病因有：1、胆红素产生增加，多见于同族免疫性溶血（ABO和Rh血型不和溶血病）：在地区因少数名族人群中Rh阴性血型者较多，因此发生Rh血型不合的溶血病较多，此类患儿黄疸出现早，程度重，进展快，伴随有肝脾肿大、贫血等症状，如不及时换血可导致死亡，即使存活易发生胆红素脑病而导致严重后遗症。

---------------------------------------------------------------最新资料推荐------------------------------------------------------第二节新生儿黄疸（Section 2 neonataljaundice）第二节新生儿黄疸（Section 2 neonatal jaundice） Section 2 neonatal jaundice Jaundice is a common clinical symptom in neonatal period. Normal serum bilirubin content was 3.4 ~ 13.7 mu mol/L (0.2 ~ 0.8mg/dl). If more than 25.7 ~ 34.2 mu mol/L (1.5 ~ 2.0mg/dl), jaundice appeared. However, neonatal skin vessels are rich in blood vessels, and the color is red, and the serum bilirubin content reaches 51.3 ~ 68.4 mu mol/L (3 ~ 4mg/dl). The occurrence of jaundice in elder or adult is pathological phenomenon, the newborn is divided by reason and pathologic two kinds. In the case of neonatal jaundice, one of the following situations should be considered as pathological jaundice: the premature death of jaundice: within 24 hours of birth, jaundice occurs within 48 hours of premature birth; Levels of jaundice: serum bilirubin is more than the normal average of the same day, or rising more than 85.5 mu per day (5mg/dl). The jaundice lasted longer (more than two weeks in the foot, more than 3 weeks for premature infants), or the jaundice was reappeared. Jaundice is accompanied by other clinical symptoms, or serum combined with bilirubin is greater1 / 19than 25.7 mu mol/L (1.5mg/dl). The characteristics of neonatal bilirubin metabolism The occurrence of neonatal biologic jaundice is related to the characteristics of neonatal bilirubin metabolism. (a) bilirubin in produce relatively excessive fetal intrauterine hypoxia environment life, red blood cell number of relatively more, if the birth time delay of umbilical cord ligation or midwives to neonatal umbilical blood from the umbilical cord, the number of red blood cells more. Fetal red blood cells have a shorter life span (70 ~ 100 days), so there are more bilirubin levels. After birth, begin to use lung respiration, blood oxygen partial pressure rises, excessive red blood cell quickly destroys, make the blood central Africa combines bilirubin to add more. Adults produce about 65.0 mu of bilirubin per day (3.8mg/kg), and the neonatal daily bilirubin is approximately 145.4 mu mol/L (8.5 mg/kg), which is twice as high as that of adults, so the load of bilirubin in newborn liver is greater than that of adults. (2) the ability of bilirubin to connect with albumin is not sufficient for the transient period after birth, and there is an acid poisoning of the severity and severity, affecting the number of bilirubin and albumin connections. The low albumin in premature infant’s blood makes the binding of bilirubin---------------------------------------------------------------最新资料推荐------------------------------------------------------ delay. (3) hepatic cell uptake of non-binding bilirubin was deficient in neonatal liver cells with a deficiency of Y protein and Z protein (only 5 ~ 20% of adults), which was gradually synthesized after the 5th day of life. These two kinds of protein with the combination of bilirubin intake, also transferred to the smooth endoplasmic reticulum for metabolic function, caused by a lack of Y and Z protein synthesis, affects the liver cells to a combination of bilirubin intake. (4) liver system development immature neonatal hepatic glucuronyl transferase and uracil nucleoside diphosphate sugar dehydrogenase (UDPG dehydrogenase) insufficient or inhibition, can’t combine the bilirubin into a combination of bilirubin, and the combination of bilirubin in the retention of blood and jaundice. Such enzymes start to increase around 1 week after birth, and premature babies are later. (5) the enterohepatic circulation increases the newborn’s first few days, and the normal flora of the intestinal tract has not been established, so the combination of bilirubin with bile enters the intestines can’t be reduced to fecal gallbladder; There are more other aspects of neonatal intestinal beta glucuronic acid glycosides enzyme, hydrolysis can be combined with bilirubin is a3 / 19combination of bilirubin, the latter is absorbed by the intestinal mucosa, via portal venous return to the liver, this is the characteristic of neonatal intestinal a hepatic circulation. The result is an increase in the burden of bilirubin in the liver, but not in the blood of bilirubin. Second, physiological jaundice The majority of newborns have yellow dye in the skin or/and mucosa 2 to 3 days after the birth, the whole body is in good condition, there is no other pathological conditions, and it lasts for about a week, which is called the physiological jaundice. (1) clinical manifestations Biologic jaundice is mostly born after the birth of two to three days, the 4th ~ 6th day is most obvious, the moon is more than 7 ~ 10 days after the birth, the premature infant can delay to the 3rd ~ 4 weeks. Jaundice is first seen in the face and neck, then can be all over the trunk and limbs, usually slightly yellow, the sclera may have light yellow dye, but the palm of the hand is not yellow. Except jaundice, Children’s health condition is good, without oth er clinical symptoms, urine color is normal. (2) laboratory inspection Normal neonatal umbilical cord blood bilirubin was up to about 51.3 mu mol/L (3mg/dl), which peaked at about 4 days after birth, generally not exceeding 171 ~ 205 mu mol/L (10 ~ 12mg/dl), and---------------------------------------------------------------最新资料推荐------------------------------------------------------ the preterm infant was not more than 256.5 mu/L (15mg/dl), and gradually recovered. There was an indirect reaction to van den’s experiment. The bilirubin was negative in the urine, and the bile pigment increased. (3) common causes and treatment of delayed extinction The reasons for the emergence of rational jaundice are multifaceted and comprehensive, so its severity and regression time are often affected by the following factors. 1. Prenatal medication: a large amount of oxytocin or vitamin K used for prenatal use. 2. There are asphyxia, lack of oxygen in labor: due to breathing difficulties, lack of oxygen, on the one hand, increased acidosis, inhibit the glucuronic acid transferase activity the other aspects, has affected the bilirubin metabolism process;3. Bleeding during childbirth can increase the bilirubin;4. After cold, hunger, can free fatty acids and other organic anions, and combined with albumin, bilirubin competition and make the bilirubin free blood, delayed feeding, meconium discharge delay, im can increase the liver circulation, increase blood china-africa combined bilirubin. In order to prevent the neonatal hyperbilirubinemia, the prenatal medication should be cautious, and the medicine can not be used5 / 19as far as possible; Intensive care during childbirth, so as to prevent fetal asphyxia and production injury; Take care to keep the newborn’s body warm and feed early. In the case of neonatal hyperbilirubinemia, treatment with phototherapy, plasma or albumin can be applied in addition to the etiological treatment. Iii. Neonatal hepatitis For starts in a set of clinical Syndrome, Neonatal period mainly for obstructive jaundice, hepatomegaly, and liver function damage, because the cause is more, for each case is difficult to determine the exact reasons, reason often called Neonatal Hepatitis Syndrome (Neonatal Hepatitis Syndrome). (I) etiology It is mainly caused by viruses such as hepatitis b virus, cytomegalovirus, rubella virus, herpes simplex virus and intestinal virus. Toxoplasmosis, lyceum, syphilis, etc., are also one of the causes of the disease. (2) clinical features The onset is slow. Jaundice occurs within days and weeks after birth and lasts longer, with symptoms such as decreased appetite, nausea, vomiting, indigestion, and weight loss. The color of the stoolis lighter, but it can be gray, but sometimes shallow and deep. The urine is dark yellow. The liver is mild to moderate and slightly hard. The few spleen are also large. Toxic hepatitisis often infected with lesions and systemic poisoning. The---------------------------------------------------------------最新资料推荐------------------------------------------------------ hepatitis caused by rubella virus and cytomegalovirus is often accompanied by congenital malformation or intrauterine growth disorder. The laboratory examined the increase of serum transaminase enzyme, the increase of bilirubin, with the combination of the increase of bilirubin, and the early change of the floccus in the floccus. The alpha-fetal protein was positive. Urinuria positive, urinuria can be positive or negative according to the degree of bile duct obstruction. To detect the surface antigen of hepatitis b virus, to collect the baby’s urine or the mother cervical spatula to find the giant cell inclusion body for the diagnosis of the etiology. (iii) treatment To protect liver treatment mainly, supply sufficient quantity of heat and vitamin. Disable drugs that are toxic to the liver. Patients with severe jaundice may use the anti-inflammatories of prednisone (2mg/kg/day) to reduce the obstruction of the bile duct, usually 4-8 weeks, to prevent other infections. The general cases can be used in qing dynasty. The etiology is clear, for the etiological treatment. Iv. Congenital biliary atresia (1) etiology The cause is unknown. It is generally believed that there is a connection with intrauterine virus infection, secondary obstruction of hepatic7 / 19hepatic ducts, and congenital biliary development. The intrahepatic bile duct, hepatic duct or bile duct can be blocked or undeveloped, and the gallbladder can be blocked or stunted.(2) clinical features 1 ~ 3 weeks after the occurrence of jaundice. And progressive aggravation. The feces can be greenish green, but soon after the birth of ash white. Severe cases of intestinal mucosal epithelial cells can seep through bilirubin, which can be stained pale yellow. The liver is enlarged and gradually hardened. Most of them have splenomegaly and the later ascites. The early disease appetite is still, the nutrition condition is mostly good; Late stage due to fat and fat-soluble vitamin absorption obstacle, the nature is gradually weak, but vitamin A, D, K deficiency causes dry eye disease, rickets and bleeding tendency. Laboratory tests, serum combined with bilirubin and alkaline phosphatase continued to increase. Early liver function is normal, late has abnormal change. Urinuria positive, urinuria negative. The condition can be used to be 99m technetium - IDA (acetanilide diacetate) imaging, and in 6 hours of the tracer, the intestines do not show a radioactive concentration, which supports the diagnosis of the disease. (iii) treatment Congenital biliary atresia should be used for surgical treatment within---------------------------------------------------------------最新资料推荐------------------------------------------------------3 months after birth. The most successful surgical success rate is the hepatic jejunostomy. However, the possibility and effect of the operation were different, and intrahepatic obstruction was difficult. 5. Hemolysis of newborn Newborns Hemolytic disease (Hemolytic diseaseof newborn) not because of the mother and the infant blood type refers to immunity hemolysis and kin. In China, the ABO blood group is not the majority, the Rh type is less, and other such as MN and Kell blood type system are rare. (1) etiology When fetal blood group antigen and which paternal inheritance from the mother is not at the same time, after entering the mother will stimulate maternal antibodies, can be through the placenta into the fetus, and fetal red blood cell antigen antibody reaction cause hemolysis. In the ABO system, there are more people with type O than type A and type B because of the O type person: A antigen is more resistant to the antigens than the B antigen, so the mother type, the foetus type A is more likely to get the disease. ABO hemolysis can occur in the first child, with the mother having been subjected to the antigenic stimulation of A and B substances in the natural world, and has been associated with anti-a or anti-b antibodies. Rh hemolytic disease of the immune antibody, can only be9 / 19produced by human blood cells as antigen stimulation and, if you did not enter the mother in childbirth fetal red blood cells, then in addition to having a history of blood transfusion rare first onset. Most people in China are Rh positive, so Rh hemolysis is rare in China. (2) clinical manifestations The severity of symptoms of the disease is significant, and the general ABO blood group is less than the Rh blood type. The disease often occurs within 24 hours or the next day jaundice, and rapidly aggravates. With jaundice, the disease of anemia, liver splenomegaly, and bilirubin brain disease occur. Rh is not a large number of hemolysis, and was born with severe anemia, which can lead to heart failure, systemic edema, and even stillbirth. (iii) diagnosis According to the clinical characteristics of jaundice and hemolytic anemia within 24 hours of birth, the diagnosis can be confirmed by combining mother, infant blood type identification and specific antibody examination. The study of serological examination and its clinical significance are shown in table 2-3. Table 2-3 hemolysis blood test project and clinical significance of neonatal hemolysis Blood serum neonatal serological examination results in the clinical significance of maternal serological examination Mother babies are directly---------------------------------------------------------------最新资料推荐------------------------------------------------------ anti-human The globulin test was indirectly anti-human The globulin test free antibody was released check O A modified + release IgG anti-a + ABO hemolysis (anti-a) O B improvement + release IgG anti-b IgG anti-b + ABO hemolysis (anti-b) Rh - Rh + + + + anti-d antibody + Anti-e antibody + Anti-c antibody + anti - D antibody There are anti-e, not perfect antibodies There is an anti-c, incomplete antibody Rh hemolysis (anti-d) Rh hemolysis (anti-e) Rh hemolysis (anti-c) (iv) treatment Measures should be taken to reduce serum bilirubin concentration and correct anemia. Drug therapy and phototherapy are commonly used. Blood transfusion is necessary. 1. Medication The main objective is to reduce serum non-binding bilirubin and prevent bilirubin encephalopathy. Chinese and western medicine can be used jointly. (1) the western medicine The plasma or albumin supply is associated with bilirubin albumin, which reduces the non-binding bilirubin and prevents bilirubin encephalopathy. Plasma 25ml/subvenous injection (100ml of plasma containing albumin 3g, 1g albumin can bind to non-binding bilirubin 8.5 mg) or albumin lg/kg plus 25% glucose 10 ~ 20ml intravenous drip, 1 ~ 2 times per day. Noil [lack of some content here] 5g, 1.5g11 / 19yellow, yellow 3g. (1) wormwood decoction, 1.5g, gardenia 9g, rhubarb 3g, licorice 1.5g. This is the most important thing in the world. The above three parties can choose one of them, daily take 1 dose, cent to feed before feeding. There is also the application of intravenous injection, which is faster than oral administration. 2. Phototherapy (1) phototherapy principle of bilirubin can absorb light, under the action of light and oxygen, fat-soluble bilirubin oxidation becomes a kind of water-soluble product (light - oxidation bilirubin, namely double pyrrole), can from in vitro bile and urine, thereby reducing not combined with serum bilirubin concentrations. Bilirubin absorption band is 400 ~ 500 nm, especially in the 420 ~ 440 nm wavelength time decomposition, the strongest blue fluorescence wavelength peaks between 425 ~ 475 nm, so much the blue fluorescent lamp for treatment. In recent years, there have been reports that the effect of green light has been better than that of the laminator. The method of phototherapy and attention should be given to the children to sleep naked in the center of the blue light box. The light s ource is 50cm from the baby’s body table, and the two eyes and genitals are covered with black cover or black cloth. Week box temperature should be kept in 30 ~ 32 ℃, anal temperature---------------------------------------------------------------最新资料推荐------------------------------------------------------ measuring 1 times per hour, keep the temperature between 36.5 ~ 37.2 ℃. Light time was determined acc ording to the etiology, severity, and serum bilirubin concentration, which can be continuously irradiated for 24 ~ 72 hours. Phototherapy has a weak effect on the combination of bilirubin. When serum is combined with bilirubin 64.8 mu mol/l (4mg/dl), transaminase and alkaline phosphatase are elevated, phototherapy of bilirubin accumulates, which can make the skin bronze, or bronze. Therefore, in combination with the combination of bilirubin, the disease of the main or liver function is not suitable for phototherapy. Blood transfusion The hematocyte and antibody were induced to prevent further hemolysis in blood exchange. Reduce serum non-binding bilirubin concentration and prevent the occurrence of bilirubin encephalopathy; Correct anemia and prevent heart failure. The hemolysis of the newborn has been confirmed in the blood exchange, and anemia, edema, hepatosplenomegaly and heart failure are at birth, and umbilical cord blood hemoglobin 120g/L. Umbilical cord blood bilirubin 59.84 ~ 68.4 mu mol/L (3.5 ~ 4mg/dl), or 6 hours after birth to 102.6 mu mol/L (6mg/dl), 12 hours to 205.2 mu mol/L (13mg/dl); The bilirubin had reached 307.8 to 342 mu mol/L13 / 19(18 ~ 20mg/dl), and the preterm neonatal bilirubin reached 273.6 mu mol/L (16mg/dl). There have been early bilirubin encephalopathy. The serum of the ABO hemolysis was selected by the serum of the serum with type AB plasma and mixed with O - type red blood cells. Rh hemolysis should have the ABO homotype (or O type), Rh negative hepatochemical blood. The source of blood should be new blood within 3 days. The amount of blood change and the usual amount of blood change was 85ml/kg, about twice the total blood of the baby. The blood volume was 10 ~ 20ml, and 10 ml of weight was taken. The speed should be even, about 10ml per minute. After changing blood can be phototherapy. To reduce or avoid another blood exchange. The operation of blood exchange is more complicated, which can cause complications such as infection, blood volume change and electrolyte disturbance. Severe anemia occurs in severe hemolysis within 2 months after birth, and should be reviewed with red blood cells and hemoglobin. If the hemoglobin 70g/L, the blood transfusion can be small. Mild anemia can be treated with oral iron. Breast milk jaundice (1) etiology Because breast milk contains more lipase and beta glucoalaldehyde, the former makes the unsaturated fatty acid in the milk increase, which inhibits the activity of the liver glucuronic acid---------------------------------------------------------------最新资料推荐------------------------------------------------------ transferase. The latter can break down the ester bonds of bilirubin glucuronate. The combination of bilirubin and bilirubin was converted into non-conjugate bilirubin, which was easily reabsorbed in the small intestine, thus increasing the intestinal - hepatic circulation, resulting in jaundice in the combination of the increase of bilirubin in the blood. Identification of jaundice in neonatal period Disease jaundice It starts with jaundice Continuous time serum bilirubin jaundice type of the type of lint physiological Jaundice was two to three days after the birth, and it was not combined with bilirubin to increase the main hemolytic and hepatic cell sex without clinical symptoms The newborn Hemolysis is 24 hours after birth The inside or the next day Or longer non-binding bilirubin increases the main hemolytic anemia, hepatosplenic, maternal and infant blood type, and severe cases of bilirubin encephalopathy Breast milk sex Jaundice is 4 ~ 7 days after 2 months The left and right non-binding bilirubin were mainly asymptomatic The newborn Blood loss is 3 to 4 days after birth Or 1-2 weeks later Or longer early non-binding bilirubin increased mainly, late combined with bilirubin increased mainly hemolytic, late and15 / 19liver cell sexual infection symptoms G - 6 - PD is less than 2 to 4 days after birth and 12 weeks Longer non-binding bilirubin is mainly hemolytic anemia, and often causes the pathogenesis The newborn A few days after hepatitis Weeks or weeks A longer combination of bilirubin and hepatic cell jaundice and defecate color have dynamic changes, GPT is elevated, and the hormone retreats yellow congenital The biliary obstruction lasts 1 to 3 weeks High and unrecombined bilirubin increases obstructive sex and liver cell sex early general condition is good late occurrence biliary cirrhosis (2) clinical features The infants who were breastfed were jaundice from 4 to 7 days after birth, and the peak of 2 ~ 4 weeks (serum bilirubin could exceed 256.6 ~ 342.0 mu mol/L) and were generally in good condition without hemolysis or anemia. Jaundice generally lasts 3 ~ 4 weeks, the 2nd month gradually subsides, a few can extend to 10 weeks. During jaundice, the jaundice decreased significantly and the bilirubin decreased by 50 %. If you use breast feeding, jaundice may not appear again, even if it appears. (iii) treatment The serum bilirubin is rarely elevated enough to produce neurotoxic levels, so there is no need to stop breastfeeding. If serum bilirubin 256.6 mumol/L should be stopped for 2 ~ 4 days, artificial feeding---------------------------------------------------------------最新资料推荐------------------------------------------------------ should be used instead. During the suspension of breast milk, the mother’s milk should be sucked out to maintain the milk secretion and ensure continued breastfeeding. In order to reduce the intestinal wall absorption of non-binding bilirubin, it can be taken by mouth 10% activated carbon solution 5ml, 1 time per hour; AGAR 125 ~ 250mg/time, 4 ~ 6 times per day. [attached] neonatal bilirubin encephalopathy Neonatal high blood not combined bilirubin occurs, free bilirubin through the blood brain barrier, deposition under basal nuclei, thalamus, hypothalamus nucleus, nucleus, ventricle, caudate nucleus, the cerebellum and the medulla, the cerebral cortex and spinal cord, in areas such as the inhibition of brain tissue of oxygen utilization, lead to brain damage, said bilirubin encephalopathy. It used to be called nucleosis. 1. Factors affecting the onset of disease (a) when the blood-brain barrier is normal, it can restrict the bilirubin into the central nervous system and have a protective effect on brain tissue. When neonatal asphyxia, hypoxia, infection, acidosis, hunger, hypoglycemia, premature birth, and the application of certain drugs, can make the blood brain barrier permeability increase, or open the combination of bilirubin into brain17 / 19tissue and produce bilirubin encephalopathy. (2) the concentration of free bilirubin in blood refers to the non-binding bilirubin that has not been linked with albumin. The higher the concentration of non-binding bilirubin, the more free bilirubin, the more than a certain limit (307.8 ~ 342.0 mu mol/L is treated as the critical concentration, and the premature infant is lower), then the blood-brain barrier can be retreated into brain cells. The other aspect, When low plasma albumin levels, acidosis, reduce the amount of coupling the bilirubin and albumin, and have capture join in albumin and bilirubin competition sites material (such as fatty acid, salicylic acid salt, sulfa, new Ⅱ and cephalothin, penicillin drugs), can be free in the blood bilirubin concentration and serum bilirubin encephalopathy. 2. Clinical manifestations The clinical phase 4 of the disease occurred in the early stage of the neonatal period from 1 to 3, and the 4th period appeared after the neonatal period. (a) the warning period is characterized by lethargy, reduced absorption reflex and hypotension. The majority of jaundice suddenly deepened significantly. It took 12 to 24 hours. (2) the spasmodic period light person gazed at only two eyes, the paroxysmal muscle tension increased; The heavy hand clench fist, the---------------------------------------------------------------最新资料推荐------------------------------------------------------ forearm, the Angle, sometimes the shrill cry. Lasts for about 12 ~ 24 hours. (3) the recovery period is mostly on the first weekend. First, the suction and response to the outside world gradually recover, and then the spasm gradually reduces and disappears. It took about 2 weeks. (4) the sequela period often occurs after 2 months or later. The expression is movement of limbs, eye movement disorder, deafness, mental retardation or tooth enamel dysplasia. Prevention and treatment For neonatal hyperbilirubinemia, comprehensive measures must be taken early in order to prevent the development of bilirubin encephalopathy. If you want to keep warm, correct hypoxia and acidosis, provide adequate nutrition. Avoid injecting high-permeability drugs, not using drugs that cause hemolysis or inhibit heparase. During the warning period, blood transfusion, phototherapy, infusion albumin and other measures were used to reduce the concentration of bilirubin in blood as soon as possible.19 / 19。