Pathologic brain anoxia

In the neonatal jaundice than any other age are common, the cause of the special and complex, both physiological jaundice, and pathological jaundice, and breast milk jaundice. These conditions should be treated differently, to deal with. If the child within 24 hours after birth jaundice or jaundice developed fast, longer duration, even accompanied by anemia, the body temperature is not normal, poor feeding, vomiting, abnormal urine color. Some have jaundice disappeared or alleviated after treatmentended and increased, mostly pathological jaundice. The common causes of pathological jaundice is hemolytic disease of the newborn, neonatal infection, biliary malformation and neonatal hepatitis.

The reason for the differential diagnosis of

brain anoxia


4.1 for the general treatment of

4.2 drugs


1 pathological jaundice causes

2 pathological jaundice diagnosis of

2.1 diagnosis of

3 pathological jaundice

4.3 light therapy

4.4 exsanguinotransfusion

5 pathological jaundice prevention at


7 reference

Pathological jaundice

Understand the parents history of pregnancy, childbirth the history of labor before have no infection and medication history, blood transfusion history, family members have no hepatitis, jaundice. Pay attention to whether there is no parity, premature birth, birth trauma, asphyxia, anoxia, hunger, infection, jaundice appeared and asked in detail about the duration and degree of fluctuation, urine color. After birth without jaundice caused by the medication history (such as sulfanilamide, salicylic acid preparation, large doses of vitamin K3, K4, etc.) and contact history (such as naphthalene mothballs etc.).Brain anoxia the diagnosis of


Pathological jaundice

Examination (1) blood count, reticulocyte count and nucleated red.

(2) determination of total bilirubin and direct bilirubin, and serum bilirubin in full-term infants up to 205 mol/L (12mg/dl) of 256 mol/L (15mg/dl) should be alert with bilirubin.

(3) urine and urinary bile three.

(4) note the color of urine, if necessary, stercobilinogen.

(5) according to the condition of selected as following:

Inspection of suspected neonatal hepatitis for liver function tests, and check the mother HB – sag, hbeag, HBV, DNA, anti hbc-igm, alpha fetoprotein (AFP positive normal newborns after birth, when january.

Suspected sepsis neonatal blood culture, local infection for smear and exudate.Brain anoxia

Suspected cytomegalic inclusion disease, urinary sediment examination for inclusion body giant cells, conditional can be used for virus isolation and serology.

Disease for suspected neonatal hemolytic test, hemolytic disease of the newborn.

Suspected of red blood cell G6PD defect detection methemoglobin reduction rate (normal 75% patients decreased); heinz body (heinz body) generation test; conditional can be used for G6PD activity.

Suspected hereditary spherocytosis, as erythrocyte fragility test (normal to 0.40% ~ 0.46% in red blood cell hemolysis, 0.30% ~ 0.36%, complete hemolysis increased brittleness.

Blood urine bancroft suspected galactose test conditions can enzyme galactose concentration and erythrocyte galactose -1- triphosphate acid determination of blood.Brain anoxia

Suspected alpha 1- antitrypsin deficiency serum protein electrophoresis test (with 1- alpha globulin 2 ~ 10/100) should check the maternal ABO and rh blood group, coombs test positive for rh incompatibility; ABO hemolytic disease in children with positive antibody release test. The test was negative or 3, 4 days after the initial onset of birth defects should be except G6PD.

(1 neonatal hemolytic jaundice disease): the start time is within 24 hours after birth or second days, for a month or more elevated bilirubin, non binding. Hemolytic anemia, hepatosplenomegaly, isoimmune patients bilirubin, serious.

(2) neonatal sepsis: jaundice start time is 3 ~ 4 days after birth or later, or for 1-2 weeks.Brain anoxia early unconjugated bilirubin increased, combined with advanced bilirubin, hemolytic, and advanced hepatocellular

, symptoms of infection (3) breast milk jaundice jaundice: the start time is after 4 ~ 7 days, lasts about 2 months with elevated bilirubin, non binding, no clinical.

(4) physiological jaundice jaundice: start time for 2-3 days, about 1 weeks of elevated bilirubin, non binding, hemolysis and liver cells, no clinical.

(5): G6PD enzyme deficiency jaundice after 2-4 days to start time, 12 weeks or longer, unconjugated bilirubin increased, hemolytic anemia, often onset.

(6): neonatal hepatitis jaundice days after birth to the start time for a few weeks, lasted for 4 weeks or longer, combined with bilirubin, obstructive and liver cells.Brain anoxia jaundice and stool color dynamic changes, the increase of GPT, hormone jaundice. No

Fecal bile pigment, dark urine, urine bilirubin and neonatal liver should be considered positive for biliary atresia, basically complete because the former often caused long intrahepatic obstruction, which is difficult to differentiate, the following checks for. Determination of serum bilirubin

Times gradually increased prompt biliary atresia, if there are fluctuations or irregular drop tips.

Serum transaminase increased significantly early college entrance examination is suggested.

Other laboratory examination of serum 5 ‘- nucleotidase significantly increased prompt biliary atresia; serum AFP 40mg/L hepatitis; duodenal fluid containing bile or bile acid can reduce external biliary atresia; lipoprotein -X (LP-X) positive suggests biliary.Brain anoxia

Intravenous 131I rose 37 ~ 148mbq (1 ~ 4 ci), 3 days (not collect feces mixed with urine) measured every minute count, such as 10% injection volume can be eliminated by biliary tract.

Radionuclide liver and gallbladder scanning the intravenous injection of 99m technetium labeled iminodiacetic acid (IDA) derivative scanning, hepatitis liver developing slowly and intestinal radioactive concentration in children with biliary atresia liver, intestinal developing occurs quickly, does not appear.

B-can found total biliary duct cyst, without gallbladder biliary tips.

Liver biopsy liver structure was normal, bile duct hyperplasia that biliary atresia; hepatic lobule structure disorders, liver cell necrosis and multinucleated giant cells to see that.Brain anoxia

Laparotomy within 2 months for the implementation, if there is no suitable for further exploration of gallbladder; gallbladder, gallbladder should be carried out, such as abnormal for hepaticojejunostomy (the earlier effect better, not later than 3 months.


General treatment

Pathological jaundice need to remove the cause, keep warm, early feeding, provide adequate calories and nutrition, adequate vitamin supplements, avoid competition with bilirubin glucuronosyltransferase or albumin binding sites for drugs, suffocation, hypoxia, acidosis, hypoglycemia and other symptoms should be timely.

Drug treatment

Enzyme inducer: to increase the glucuronosyltransferase generation and liver uptake of unconjugated bilirubin, commonly used phenobarbital, lo for the first 15mg / kg intramuscular injection 8 12h after failure, the daily 5 mg / kg, 2 – 3 oral, 4-5d, is also available; can brake meters daily 100 mg / kg, 2 – 3 oral, 4 -.Brain anoxia

Albumin: jaundice serious infusion of albumin or plasma, can reduce the free unconjugated bilirubin, and reduce the occurrence of bilirubin encephalopathy, intravenous albumin or plasma 1g / kg, each lo.

Intravenous immunoglobulin: blocking the mononuclear phagocyte system FC receptor, inhibition of phagocytic cells to destroy zhi minhong, usage: LG / kg, 6 – 8 h intravenous drip. Objective to evaluate the clinical effect of early application, due to immunoglobulin only reduce hemolysis, can reduce the level of bilirubin has been produced, so it needs to be combined with phototherapy and other measures.

Metalloporphyrins: tin protoporphyrin, zinc protoporphyrin, tin porphyrin, zinc porphyrin can inhibit the production of bilirubin, non-toxic.Brain anoxia

: dexamethasone for severe neonatal hemolytic disease, early intravenous injection of dexamethasone daily 0.3 – 0.5mg / kg, 2 -.

Hepatoprotectants: neonatal hepatitis drug available, such as glucurolactone 25-50mg, 2 / D, mg / 0.5 biphenyldicarboxylate every time. 2 – 3 / D taking two glycyrrhizic acid amine or glycyrrhizin daily 1 – 1.5ml / kg intravenous drip, 10 – 14D.

Anti infection: herpes simplex virus, cytomegalovirus infection can be 10 15mg / (kg – D), 2 – 3 or 10 mg intravenous ganciclovir / kg, intravenous infusion of 2 lo, continuous 14d, hepatitis B virus interferon – 1 million U / 50 available time, intramuscular injection, 2 a week 3 times for 3 – 6 months, if choose sensitive antibiotics bacterial infection.Brain anoxia

Montmorillonite powder: montmorillonite powder 1.5g 8 h every time, one time, with 10% glucose 15 iill mixed feeding treatment of breast milk jaundice, effect.

Treatment: yinzhihuang injection or oral liquid, liver jaundice, but bitter in the blood can replace bilirubin and albumin, free bilirubin, bilirubin encephalopathy may have induced, of the newborn.

Light therapy is not the

Reduce serum bilirubin of simple and effective method, the wavelength of blue light and 425 – 475nm 510 to 530nm wavelength green light effect. Phototherapy mainly acts on the shallow layer of the skin, so the skin jaundice does not necessarily indicate serum unconjugated bilirubin fell to normal. When phototherapy should be added riboflavin, water and calcium.Brain anoxia such as serum total bilirubin in 2 consecutive 185nmol / L non hemolytic jaundice phototherapy can stop. Most intermittent irradiation. The continuous irradiation of 8 – 12h 16 h or 12h irradiation stop. Research shows that intermittent irradiation effect with continuous irradiation, but the former can significantly reduce the adverse effect of phototherapy.


For most of rh hemolytic disease and severe hemolytic disease of individual ABO, can change the part of blood and free antibody sensitized red blood cells, reduce hemolysis in a large number of bleeding and prevent the occurrence of bilirubin, bilirubin encephalopathy, correction of anemia, improve oxygen, prevent. The

brain anoxia

Pathological jaundice prevention

(1) taihuang due to maternal and fetal suffering from damp heat invasion involved, resulting in fetal birth appear yellow, so during pregnancy, pregnant women should pay attention to diet, but eat cold, but hunger and satiety, and avoid alcohol and xin heat of the goods, in case.

(2) who had a pregnancy women yellow baby, then the pregnancy should be taken in time to prevent.

(3) infants born after close observation of the sclera jaundice, jaundice found should be treated as soon as possible, and to observe the color change to understand jaundice jaundice.

(4) to observe the fetal baby’s symptoms are yellow, listlessness and somnolence, suckling difficulties, restlessness with fear, two eye strabismus, limb rigidity or convulsions and other symptoms, so that children with severe early detection and timely.Brain anoxia

(5) close observation of heart rate, heart rate and the size of the degree of anemia and liver changes, early prevention and treatment.

(6) pay attention to the protection of the baby skin, umbilicus and buttocks clean, prevent breakage.

(7) required blood transfusion therapy, should be timely ward air disinfection, prepare blood and various drugs, items, strict operation.


Breast milk jaundice neonatal hepatitis



Drug jaundice

Erythrocyte glucose – -6- phosphate dehydrogenase (G-6-PD) deficiency

Biliary atresia

Septicemia of newborn hemolytic disease of the newborn

Coital jaundice

Congenital non hemolytic jaundice of newborn

Persistent cholestatic jaundice

Physiological jaundice of newborn

brain anoxia

Acholuric jaundice syndrome


Breast milk jaundice syndrome

Duodenal diverticulum obstructive jaundice comprehensive

Neonatal jaundice

Systemic symptoms


Pediatrics people’s medical publishing house 7th medical textbook, edited by wang weiping shen xiaoming. The etiology and treatment of neonatal pathological jaundice.

Shandong medicine ISTIC PKU -2009 33 meters