1.Is the yellowing of the newborn’s skin jaundice?
Basically, yes.
Strictly speaking, neonatal jaundice should be called neonatal hyperbilirubinemia, and the diagnosis must be confirmed by the presence of “elevated bilirubin values”, which in turn leads to yellowish staining of the skin and sclera (i.e., the whites of the eyes).
However, it is very unlikely that a newborn’s skin will become yellow due to other factors, such as diet, so when a newborn’s skin gradually becomes yellow, it is basically certain that it is due to elevated bilirubin and can be called neonatal jaundice.
2. Does jaundice occur in all newborns?
Neonatal jaundice is one of the common symptoms of the newborn period. Under normal circumstances, jaundice can be observed visually in about 80% of full-term infants.
In newborns, due to the lack of their own bilirubin metabolism, there is always a certain degree of bilirubin accumulation in the blood during the first 1-2 weeks of life; in newborns, we can see the yellowing of the skin (i.e. jaundice) with the naked eye when the total bilirubin value in the blood is >85 μmol/L (5 mg/dl).
3. How is neonatal jaundice classified?
Most commonly used clinically, there are two methods of classification.
(1) According to the cause of jaundice, it can be classified as
Physiologic jaundice; (see Q8 for details)
pathological jaundice (which includes jaundice caused by various types of pathological factors, such as breast milk jaundice, neonatal hepatitis syndrome, etc.)
(2) According to the degree of elevated bilirubin levels in the blood, they can be classified as
severe hyperbilirubinemia (peak TSB >342umol/L, i.e. 20 mg/dl)
very severe hyperbilirubinemia (TSB > 427umol/L, i.e. 25 mg/dl).
Dangerous hyperbilirubinemia (TSB>510umol/L, i.e. 30 mg/dl), except for those classified as mild or moderate.
4.What tests are available to help diagnose the severity of jaundice?
(1) Total serum bilirubin (TSB): It is the gold standard for the diagnosis of hyperbilirubinemia (i.e., the test that most visually and accurately reflects the level of bilirubin in the blood) and is the sum of direct bilirubin (conjugated bilirubin) and indirect bilirubin.
(2) Transcutaneous bilirubin value (TcB): a non-invasive test, which can be measured by shining a light on the skin with a jaundice meter.
5.What is the difference between direct bilirubin and indirect bilirubin?
The essence of the difference between the two lies in whether or not the bilirubin has been successfully “modified” by the liver, with indirect bilirubin being the original state and direct bilirubin being the modified state.
Before bilirubin passes through the liver, it is free in the blood and is called unconjugated bilirubin (i.e. indirect bilirubin), which is fat-soluble and insoluble in water, and thus cannot be excreted through the kidneys and bile.
Once it has been “transformed” by the liver, it becomes water-soluble and can be excreted through the urine and stool due to “amalgamation” with other substances.
Most clinical cases of neonatal jaundice are mainly due to elevated indirect bilirubin. If the direct bilirubin value in the blood is significantly elevated, it is necessary to be alert to hepatobiliary problems.
6.When does jaundice usually begin to appear in newborns?
There are some differences between physiological jaundice and pathological jaundice.
(1) Physiologic jaundice usually starts 2-3 days after birth and peaks in 4-5 days (transdermal bilirubin value ≤12.9 mg/dl) and lasts for about 7-10 days to subside.
(2) Pathological jaundice may appear earlier (within 24 hours after birth), faster (rising more than 5 mg/dl per day), higher (generally >12.9 mg/dl), and more persistent (jaundice often lasts more than 2-4 weeks and even does not subside for a long time).
Of course, the above criteria are not invariable, for example, physiologic jaundice in preterm infants may be earlier, higher, and more persistent than in normal full-term infants.
7.What is physiological jaundice? How to confirm the diagnosis?
Physiologic jaundice is a normal phenomenon in the development of newborns, and its bilirubin elevation is transient and temporary, and can often disappear on its own.
However, because there are so many factors affecting the degree of jaundice, it is difficult to have a unified diagnostic standard for physiological jaundice, which can only be an exclusive diagnosis and can only be confirmed after pathological factors have been completely excluded.
Commonly used physiological normal values are: transcutaneous bilirubin value <12.9 mg/dl for term infants; <15.0 mg/dl for preterm infants.
8.Why does physiologic jaundice occur?
The production of jaundice is directly related to its source and transport process. Neonatal jaundice is very much related to the specificity of the red blood cells, liver and intestinal function of the newborn.
(1) Bilirubin is generally produced because red blood cells have a life span and are constantly produced, and bilirubin is produced after decomposition. The life span of red blood cells in newborns is much shorter (about 70-90 days compared to 120 days in adults), and the number of red blood cells is too high, making too much bilirubin production.
(2) The bilirubin produced by the decomposition of red blood cells above is indirect bilirubin, which is “transformed” by the liver into direct bilirubin before it can be excreted. The immature function of the liver in newborns leads to a low ability to “transform” unconjugated bilirubin, which results in slow bilirubin excretion.
(3) Enterohepatic circulation: Briefly, some of the bilirubin is recycled back into the blood before it is excreted in the stool. Neonates tend to have much more of this recycled than adults due to imperfect intestinal function.
(4) Poor albumin function: During the metabolism of bilirubin, albumin acts as a truck to transport indirect bilirubin to the liver for “transformation”. In contrast, there is often a deficiency in the capacity and quantity of albumin in the newborn, which in turn leads to reduced bilirubin excretion.
9.Does physiological jaundice require treatment?
(1) For normal full-term infants, physiological jaundice does not require special treatment and most of it can subside on its own. However, as mentioned earlier, physiological jaundice is an exclusive diagnosis and you can never be sure that it is physiological until other pathological factors are ruled out, so you still need to closely monitor the changes in the jaundice value and once it exceeds the normal value, it is best to visit the hospital to improve the relevant tests to rule out pathological factors.
(2) In preterm infants, prematurity itself is a high-risk factor. Therefore, the TSB (total serum bilirubin) of preterm infants needs to be treated in advance, even if it is within the normal range.
10.What are the causes of pathological jaundice?
(1) Excessive bilirubin production: such as excess red blood cells or hemolysis (the most common is ABO hemolysis, others are caused by other damages such as RH hemolysis, C6PD enzyme deficiency, red blood cell defects), hemorrhage (such as cranial hematoma, intracranial hemorrhage, visceral hemorrhage, etc.), infection (which can lead to red blood cell destruction), etc.
(2) Decreased ability of the liver to process bilirubin: for example, impaired liver function such as neonatal hepatitis, infection, asphyxia, hypoxia, hypothyroidism, bile duct atresia, drug damage, etc., can affect the liver’s processing of bilirubin.
(3) Increased intestinal and hepatic circulation: such as congenital intestinal atresia, intestinal obstruction, breastfeeding, starvation, etc.
11.Does breast milk also cause jaundice? Why?
It will. The causes of jaundice caused by breastfeeding are not yet completely clear, but the more accepted theory is “increased enterohepatic circulation in newborns”.
(1) In newborns who are exclusively breastfed, there is a delay in the excretion of feces due to insufficient breast milk intake in the early days of life (first 3-5 days), which leads to a decrease in bilirubin excretion.
(2) Breast milk contains more β-glucuronidase (β-GD), which causes the rehydration of conjugated bilirubin in the intestine to unconjugated bilirubin, which is then “recycled” by the liver, increasing the enterohepatic circulation and causing jaundice to increase.
These are the two main causes.
12. What is the difference between breast milk jaundice and physiological jaundice?
Breast milk jaundice can be divided into two categories: early-onset and late-onset jaundice (the following are based on full-term infants)
(1) Early-onset breast milk jaundice: It occurs within 1 week after birth, and its time of appearance (2-3 days after birth) and time of peak (4-5 days after birth) are similar to physiological jaundice; however, its peak is higher than that of physiological jaundice (TSB>12.9 mg/dl), and the duration of jaundice is longer (generally it can be extended to 3 weeks).
(2) Late onset breast milk jaundice: It usually occurs 1-2 weeks after birth, the TSB (total serum bilirubin) value will exceed the physiological range, the peak of jaundice occurs 2-3 weeks after birth, and the jaundice lasts 4-6 weeks, or even 2-3 months.
13. How is breast milk jaundice diagnosed?
At present, there is a lack of visual laboratory tests to confirm the diagnosis of breast milk jaundice. The diagnosis relies mainly on the following points.
(1) being an exclusively breastfed or predominantly breastfed newborn.
(2) manifestations of jaundice consistent with breast milk jaundice.
(3) Good general condition with normal growth and development.
(4) The most important thing is that after 3~5 days of stopping breastfeeding, the jaundice of the child subsides significantly and the blood bilirubin value decreases rapidly by 30%~50%.
14.Does breast milk jaundice need to be treated? How to deal with it?
The prognosis for breast milk jaundice is generally considered good, and the jaundice can subside on its own by suspending breast milk or continuing breastfeeding. The current domestic recommendations for the management of breast milk jaundice are as follows.
(1) Early-onset breast milk jaundice: It is mainly considered to be due to insufficient energy intake in the early stage, so we should encourage small and repeated feedings to ensure sufficient breast milk and energy intake, and supplement formula if necessary; at the same time, we should actively monitor the bilirubin value (inpatient monitoring is recommended), and early intervention is needed if the intervention criteria are met.
(2) Late onset breast milk jaundice: If TSB <15 dl="">15 mg/dl, suspend breast milk for 3 days and switch to artificial feeding; if >20 mg/dl, additional phototherapy is needed.
15.Can a child diagnosed with breast milk jaundice continue to breastfeed after the jaundice has subsided? Will it rise again?
Yes, jaundice can reappear, but as the child’s intestines gradually adapt, the jaundice is often lighter than before.
16.Will probiotics help my baby’s jaundice go down?
The role of probiotics is to improve the intestinal environment, regulate and improve the intestinal flora, and a normal intestinal flora helps to transform the conjugated bilirubin into fecal bilirubin (part of the stool), which is then eliminated from the body, thus reducing the enterohepatic circulation. So, the effect is there.
However, if the child’s own intestinal tract is sufficiently well-functioning, this does not really help much.
17. What are the dangers of jaundice? Is it damaging to the baby?
In addition to the cosmetic changes, jaundice can cause damage to the newborn on two levels.
(1) Primary disease: For children with pathological jaundice, those “pathological factors” that cause a rise in jaundice are a danger in themselves, such as hemolysis, hepatitis, infection, etc. These need to be treated.
(2) Bilirubin encephalopathy: the greatest damage caused by bilirubin to babies, which must be actively prevented and treated. (See 19, 20 questions for details)
18.What is bilirubin encephalopathy? How does it happen?
There is a protective umbrella in our brain (called the blood-brain barrier) that serves to limit the entry of certain substances into the central nervous system, which can cause damage to the nervous system.
However, bilirubin (exactly free bilirubin also known as indirect bilirubin) is allowed to enter. Under normal circumstances, the free bilirubin level in the blood is not high and does not enter much, so it does not cause damage to the brain.
However, when severe jaundice occurs, a large amount of free bilirubin enters the central system; and bilirubin has a toxic effect on cells, which can damage the cells of the central nervous system, which in turn causes neurological dysfunction (such as motor, hearing, learning disorders), which is called bilirubin encephalopathy.
19.What are the manifestations of bilirubin encephalopathy?
The symptoms of typical bilirubin encephalopathy are summarized in 4 stages; the first 3 stages are collectively called acute bilirubin encephalopathy, and the last stage is called chronic bilirubin encephalopathy.
(1) Warning stage: 1 to 3 days after birth, low response, low muscle tone, poor feeding, etc.
(2) Spasticity: irritability (i.e., easily frightened), refusal of milk, suspension of whistling, and high muscle tone (typical expression is corneal inversion); in severe cases, coma or even death can occur.
(3) recovery period: generally 1 week after birth, the previous symptoms gradually disappear and return to normal.
(4) Sequelae period: Most of them start to appear one after another before the age of 1 year, manifesting as motor disorders, hearing loss, difficulty in turning the eyes, abnormal dental development, etc.
In reality, many children with bilirubin encephalopathy have symptoms that are not completely typical as above due to interventional treatment, and it may only show some of the symptoms.
20.Which children are prone to bilirubin encephalopathy?
(1) Children with more than severe hyperbilirubinemia (total serum bilirubin is often above 342.2umol/L, i.e. >20 mg/dl);
(2) Although the blood bilirubin index is not severe or above, those with risk factors such as prematurity, hypoxia, dehydration, hypoglycemia, infection, acidosis, etc., are also prone to bilirubin encephalopathy. The main reason is that in these cases, the permeability of the blood-brain barrier increases and bilirubin enters more easily.
21.Can bilirubin encephalopathy be treated?
In children with acute bilirubin encephalopathy (first 3 stages, see Q20), the most important thing is to lower the bilirubin level as quickly as possible. In these children, even if bilirubin encephalopathy has already occurred, reversal of neurological damage is possible if bilirubin values can be reduced rapidly.
And once the posterior phase is reached, only intelligent and motor rehabilitation can be actively carried out.
22.Can bilirubin encephalopathy be prevented?
The prevention of bilirubin encephalopathy mainly lies in actively lowering bilirubin levels while minimizing the occurrence of high-risk factors by.
(1) Prevent preterm birth and obstructed labor as much as possible through good prenatal checkups.
(2) Do not abuse vitamin K and sulfonamides during the perinatal period.
(3) Active monitoring of jaundice in newborns within 72 hours of birth, and timely intervention once the intervention index is reached.
(4) Early diagnosis and treatment of neonatal hemolytic disease.
(5) timely correction of asphyxia, hypoglycemia, acidosis and infection, etc.
23.What are the treatment methods for jaundice?
Including light therapy, blood exchange therapy, drug therapy.
24.Why can light reduce jaundice?
In layman’s terms, light can make the bilirubin “deformed”. The bilirubin in the blood is insoluble in water, but after it is “deformed”, it becomes soluble, so it can be excreted through bile and urine without the “transformation” of the liver, which speeds up the removal of bilirubin.
25. What kind of light is used in light therapy? Is it the same as sunlight?
At present, the most commonly used light source is blue light, mainly because the light absorbed by bilirubin has the strongest effect with the wavelength of 450~460nm, and the wavelength of blue light is 425~475nm, which is the most suitable for the requirement.
Sunlight contains a variety of different wavelengths of light, of which there is of course blue light, so the sun has a certain degree of help to reduce jaundice.
26. Since sunlight is also effective in reducing jaundice, is it enough to get more sunlight at home?
The effect of light therapy is positively related to the exposed skin area, the intensity of the light and the duration of the light. If you sunbathe at home, it is difficult to ensure all three of these things, which is a drop in the bucket for a child who needs to actively reduce jaundice.
Secondly, the ultraviolet rays of the sun may also cause skin damage.
Therefore, for children with high jaundice and rapid rise, sunlight alone is not advisable.
27.How long does phototherapy usually take?
Phototherapy is divided into continuous and intermittent irradiation.
(1) continuous irradiation is mainly used for patients with heavy jaundice hemolysis (such as ABO hemolysis, RH hemolysis), which can last 24-72 hours.
(2) Intermittent irradiation: after 8-12 hours of irradiation, stop for 12 or 16 hours and cycle again.
For general hyperbilirubinemia patients, the light duration of 24~48 hours can obtain satisfactory results.
28.Does phototherapy have side effects?
Yes, there are.
(1) Fever: mainly due to the heat production of the blue light box itself, just pay attention to ventilation.
(2) diarrhea, rash: generally can be relieved after stopping phototherapy.
(3) Light during phototherapy can cause damage to the retina, and prolonged intense phototherapy increases the risk of male infants with squamous carcinoma of the external genitalia. Therefore, it is important to cover both eyes with light-blocking eye shields and cover the perineum with diapers while exposing other parts of the skin as much as possible during phototherapy.
29.What is bronchiectasis?
A child with jaundice whose skin, serum, and urine turn bronze after phototherapy is called bronchitis.
Bronchitis occurs only in children with cholestasis, and the exact mechanism is unknown. Apart from the change in appearance, there are usually few other adverse effects and there is no cause for concern. Bronchiectasis can gradually subside after phototherapy is stopped.
30. What is blood exchange therapy?
In patients with indications for blood exchange, red blood cells and plasma from another person (to be matched with the child’s blood) are used to replace almost all of the child’s own red blood cells and plasma, with the following aims.
(1) timely exchange of antibodies and sensitized red blood cells to reduce hemolysis.
(2) Reduce the concentration of bilirubin in the serum to prevent the development of bilirubin encephalopathy.
(3) To correct anemia and prevent heart failure.
31.When is blood exchange needed?
Blood exchange therapy is the most rapid method to treat hyperbilirubinemia. The indications for blood exchange are as follows.
(1) Clearly severe hemolysis with HB<110 g/L with edema, hepatomegaly, heart failure, etc.
(2) newborns whose serum bilirubin values meet the criteria for blood exchange and who have poor phototherapy results; (this criterion varies with the age and weight of the child and needs to be analyzed on a case-by-case basis)
(3) For patients who already have symptoms of acute bilirubin encephalopathy, blood exchange is recommended regardless of whether the bilirubin value exceeds the standard.
32. Is blood exchange a permanent solution, and is there any other treatment needed?
After blood exchange, the child does not need to worry about the following aspects.
(1) In some children, bilirubin may rebound 2 to 4 hours after blood exchange, so phototherapy should be continued and TSB (total bilirubin) should be monitored every 4 hours.
(2) Prophylactic antibiotics to prevent infection within 3 days after surgery.
(3) Monitor electrolytes, blood gas and blood glucose to correct abnormalities in a timely manner.
(4) If the serum bilirubin value still does not reach the index of blood exchange after blood exchange, a second blood exchange is required.
33.What are the common clinical drugs used to treat jaundice?
(1) Enzyme inducers: commonly used is phenobarbital, which increases the ability of hepatocytes to process unconjugated bilirubin.
(2) Albumin: mainly used to bind free bilirubin and prevent the occurrence of bilirubin encephalopathy.
(3) Intravenous immunoglobulin: mainly used in patients with hemolysis to block the hemolytic process.
34.Why can’t children with jaundice receive vaccination?
Because the presence of jaundice in the child itself indicates that the child is in an abnormal and weak state; at this time, the vaccination may be infected by the vaccination, so it needs to be avoided as much as possible.
For children with jaundice who have not been identified with definite adverse factors, it is recommended to wait for the jaundice to subside before administering the vaccination; delaying the vaccination will not affect the effectiveness of the vaccine.