Analysis:
Jaundice is a phenomenon of yellow staining of skin and sclera caused by the increase of bilirubin in the body. Neonatal jaundice is more common, lead
There are many and complicated causes, which can lead to bilirubin encephalopathy (nuclear jaundice) and often lead to death or serious sequelae.
Metabolic characteristics of neonatal bilirubin
1. Newborns with more bilirubin produce more than twice as much bilirubin as adults every day, which is due to newborns.
There are relatively many red blood cells at birth; Its life span is 20 ~ 40 days shorter than that of adults, and it is destroyed quickly. Bypass bilirubin comes from many sources and blood.
The content of lycopene oxygenase is high within 7 days after birth, which has great potential to produce bilirubin.
2. Liver cells with immature liver function have low Y and Z protein content and poor bilirubin uptake ability, which can reach 5 ~ 15 days.
Adult level; The quantity and activity of uridine diphosphate glucuronosyltransferase (UDPGT) in liver cells are insufficient, which leads to its formation.
The binding bilirubin function is poor.
3. The normal flora in the intestine of newborns with special enterohepatic circulation has not been established at birth, and the bile entering the intestine cannot
Lycopene is converted into urobilinogen in urine and urobilinogen in feces. What about the intestines of newborns? -High glucuronidase activity can cause intestinal obstruction.
Conjugated bilirubin is hydrolyzed into glucuronic acid and unconjugated bilirubin, which is absorbed by intestinal wall and reaches the liver through hepatic portal vein. aggravate
The burden of the liver.
Therefore, the ability of newborns to absorb, combine and excrete bilirubin is only 1% ~ 2% of that of adults, which is prone to jaundice.
Classification of neonatal jaundice
(1) physiological jaundice
Most full-term infants develop jaundice in 2 ~ 3 days after birth, and the jaundice is the heaviest in 5 ~ 7 days, and it subsides in 10 ~ 14 days, which can be delayed for premature infants.
As late as 3 ~ 4 weeks, it is generally in good condition. Serum bilirubin
At present, the upper limit of jaundice is considered inappropriate, because even bilirubin
Bilirubin encephalopathy.
(2) Pathological jaundice
1 features jaundice within 24 hours; ② Jaundice is severe and develops rapidly, with serum bilirubin > 205 umol/L (65438 02 mg
/dl) or daily increase of > 85 umol/l (5 mg/dl). ③ The duration of jaundice is too long (term infants > 2 weeks, premature infants > 4.
Week) or retired and reappeared, and gradually increased; ④ serum bound bilirubin > 26 umol/l (1.5 mg/dl).
2. the reason
(1) infectivity: ① neonatal hepatitis, which is mostly caused by the transmission of virus to fetus through placenta or infection through birth canal.
Cytomegalovirus and hepatitis B virus are common; (2) Neonatal sepsis and urinary tract infection, due to bacterial toxins to accelerate the red.
Caused by cell destruction and liver cell damage.
(2) Non-infectious: ① hemolysis of newborn (see this section); ② Biliary atresia; ③ Breast milk jaundice; ④ Delayed meconium
Discharge; ⑤ Hereditary diseases, such as glucose 6- phosphate dehydrogenase (G6PD) deficiency in red blood cells; ③ Drug-induced jaundice is like vitamins.
Su Sheng K. and so on; ① Others such as hypoglycemia, acidosis, hypoxia, internal bleeding and dehydration can aggravate jaundice.
Principles of treatment
1. Find out the reason and take corresponding treatment measures.
2. Blue light therapy reduces serum bilirubin (see Chapter 5, Section 5); Feed early and keep the stool unobstructed.
3. Protect the liver and control infection. Do not use drugs that are harmful to the liver and may cause hemolysis and jaundice.
4. Correct transfusion of plasma and albumin to prevent bilirubin encephalopathy.
5. Correct hypoxia and water-electrolyte disorder, and maintain acid-base balance.
Second, hemolytic disease of newborn
Hemolytic disease of newborn refers to blood group incompatibility between mother and infant, and maternal blood pair.
The immune antibody IgG of fetal red blood cells enters the fetal circulation through the placenta, and the same immune reaction occurs, resulting in the fetus and newborn.
Hemolysis caused by the destruction of red blood cells.
At present, there are more than 60 blood group antigens with known etiology and pathogenesis, but ABO blood group is a hemolytic disease of newborn.
System incompatibility is the most common, followed by Rh blood group incompatibility. Mainly because the blood types of mother and fetus are incompatible.
Blood group antibody (IgG) can enter fetal circulation through placenta, causing fetal red blood cell destruction.
And hemolysis occurs.
(1) ABO blood group incompatibility
Mothers are mostly type O, babies are type A or B, mothers are type AB or babies are type O, and hemolysis will not occur. ..
Due to the widespread existence of blood group A and B substances in nature, women with type O blood usually have been exposed to blood groups A and B before pregnancy.
The antigen substance of blood group substance * * * produces corresponding IgG antibodies against A and B in its serum.
Placenta enters the fetal blood circulation and causes hemolysis, so about 50% of people with ABO blood group incompatibility can get sick in the first child.
(2) Rh blood group incompatibility
Rh blood group has six antigens (c, c; d、d； E, e), in which D antigen was first discovered and has the strongest antigenicity.
Clinically, all D antigens are called Rh positive, and vice versa. Most Han people in China are Rh positive, only 0.34%.
It's Rh negative
When the Rh blood group of fetal red blood cells is incompatible with the mother's, if the mother really lacks the antigen of fetal red blood cells,
Once the fetal red blood cells are delivered, the placenta loses blood and enters the maternal circulation, which makes the mother produce corresponding blood group antibodies. Since the beginning
When the second mother is sensitized, the immune response develops slowly, producing IgM-type weak antibody, which cannot pass through the placenta and will be produced later.
When IgG antibody is used, the fetus has already given birth, so 1 fetus will not have Rh hemolysis. When the first reaction occurs,
When the mother is pregnant again in the later stage, even if the fetal blood volume entering the mother during delivery is very small (0.0 1 ~ 0. 1ml), it can be very fast.
The second rabbit epidemic often occurs, producing a large number of IgG antibodies, which enter the fetus through the placenta and cause hemolysis. So Rh hemolysis
With the increase of parity, the symptoms become more and more serious. Very few mothers who have not received blood transfusion will have Rh hemolysis when they are pregnant with 1 fetus.
The disease may be related to the fact that the maternal is Rh negative and the maternal mother is Rh positive.
Rh blood group incompatibility hemolytic disease mainly occurs in Rh negative pregnant women and Rh positive fetuses, but it can also occur in mothers and babies at the same time.
Positive results are mainly caused by anti-E, anti-C or anti-E, anti-C, etc. Among them, anti-e is more common.
The severity of clinical symptoms, the amount of IgG antibody produced by the mother and the degree of binding between the antibody and fetal red blood cells.
And fetal compensatory ability. There are great clinical differences in ABO hemolysis, and Rh hemolysis is often more serious than ABO hemolysis.
1. Fetal edema The baby was born with edema, pale skin, ascites, hepatosplenomegaly and poverty.
Hemorrhagic heart failure, if not rescued in time, most of them die, and severe cases are stillbirth.
2. Jaundice Rh hemolytic patients usually appear jaundice within 24 hours, and ABO hemolytic disease usually appears 2 ~ 3 days after birth.
Jaundice develops rapidly.
3. Anemia Rh hemolysis, generally anemia appears early and serious; ABO hemolytic patients have less anemia, which usually occurs after the newborn.
The period didn't appear. Severe anemia is prone to anemia heart failure.
4. Bilirubin encephalopathy refers to the brain mass caused by free bilirubin through the blood-brain barrier.
Pathological damage of tissues, also known as nuclear jaundice. It usually occurs 2 ~ 7 days after birth, especially in premature infants.
Vitamin > 342 umol/L (20 mg/dl) is easy to cause nuclear jaundice and needs active treatment.
Principles of treatment
1. Prenatal treatment can adopt plasma exchange for pregnant women, intrauterine blood transfusion and consider early delivery.
2. Postpartum treatment includes exchange transfusion therapy, blue light therapy (see Chapter 5, Section 5), anemia correction and symptomatic treatment.
(Plasma and albumin can be infused to correct acidosis and hypoxia, strengthen warmth and avoid rapid infusion of hypertonic drugs).
Third, the nursing of neonatal jaundice
Common nursing diagnosis
1. Activity intolerance is related to anemia caused by massive destruction of red blood cells.
2. Potential complications, bilirubin encephalopathy is related to bilirubin passing through the blood-brain barrier.
3. Lack of knowledge (parents) is related to lack of knowledge about jaundice.
Nursing measures
(A) to understand the degree of jaundice
1. Observe the skin. According to the location and range of children's skin yellow staining, serum bilirubin is estimated and its development speed is judged.
2. Phototherapy care (see Chapter 5, Section 4)
3. Patiently feeding children with jaundice often shows weakness in sucking and poor appetite. Nurses should adjust the feeding prescription as needed.
Such as a small number of times, intermittent feeding, etc. To ensure the intake of milk.
(2) Close observation
1. Observe body temperature, pulse, breathing and bleeding tendency with vital signs, especially when blue light is irradiated, and strengthen monitoring.
Measure the number of times, keep warm, ensure the stability of body temperature, find the respiratory changes in time and deal with them actively.
2. The nervous system mainly observes the crying sound, sucking force and muscle tension of children. So as to judge the occurrence of non-nuclear jaundice.
3. Observe the frequency, quantity and nature of defecation. If meconium is delayed, enema is needed.
Enter the stool and excrete bilirubin.
4. Treat the infected focus, and observe whether the skin and infected focus are damaged or not, and whether there is secretion in the navel. If there is any abnormality, handle it in time.
Handle.
5. Rehydration management Arrange the rehydration plan reasonably and correct acidosis in time. It varies according to the content of rehydration.
Speed, avoid rapid infusion of hypertonic drugs, so as not to temporarily open the blood-brain barrier, so that bilirubin has been linked to albumin
It can also enter brain tissue.
(3) Health education
(1) Make parents know about the illness and get parents' cooperation; ② For neonatal hemolysis, prenatal consultation and pregnant women should be done well.
Preventive medication; ③ Patients with bilirubin encephalopathy should pay attention to the occurrence of sequelae and give rehabilitation treatment and nursing. ④ If yes.
Breast milk jaundice can continue. If jaundice still appears after breast-feeding, breast-feeding can be changed to interval.
Go to normal breastfeeding. If the jaundice is serious and the child's general condition is poor, you can consider suspending breastfeeding. After jaundice subsided,
Then resume breastfeeding. ⑤ In the case of G6PD deficiency in red blood cells, it is necessary to avoid eating broad beans and their products. When taking care of children's clothes,
Do not put mothballs, and pay attention to the choice of drugs, so as not to induce hemolysis.