The essence of jaundice that people see with the naked eye is “bilirubin”. When bilirubin is retained in the body, serum bilirubin increases and yellowing of the skin, mucous membranes or other organs occurs. Therefore, “yellow” is not necessarily jaundice, such as yellowing of the skin after eating too many oranges.
Sources of bilirubin
1, hemoglobin from aging red blood cells: the life span of red blood cells in normal human blood is 100 to 120 days, and about 1% of red blood cells die of aging every day. The bilirubin from hemoglobin decomposition accounts for about 80% of the source of bilirubin.
2, hemoglobin containing hemoglobin in the liver or other tissues.
Metabolic characteristics of neonatal bilirubin
Neonates have a large number of red blood cells and a short life span (less than 70 days for preterm infants and about 80 days for term infants), which produce more bilirubin; the ability of liver cells to take up and process bilirubin is low, and the bilirubin excreted into the intestine is heavily reabsorbed – the enterohepatic cycle, so neonates are prone to bilirubin retention in the body –Jaundice, medically known as “neonatal jaundice”.
Under normal circumstances, jaundice can occur in 60% of full-term infants, while the incidence in premature infants is over 80%. If the jaundice appears 2~3 days after birth, reaches its peak in 4~6 days, total serum bilirubin is less than 221~256μmol/L, jaundice disappears within 2 weeks after birth in full-term infants (total serum bilirubin is less than 17μmol/L), disappears within 3~4 weeks in preterm infants, and is generally in good condition, it is called “neonatal physiological jaundice “and does not require treatment. If the jaundice appears within 24 hours after birth, if the jaundice is excessive, if it does not subside or if it recedes but reappears, then pathological jaundice should be considered and a pediatrician should be consulted.
If the fetus is born with a cranial hematoma due to head compression, the absorption process expands the source of bilirubin in the body, which may aggravate the “physiological jaundice” and delay its remission, leading to a misjudgment of “pathological jaundice”.
Although total serum bilirubin <256 μmol/L in preterm infants is a physiological value, bilirubin encephalopathy may occur, leaving a lifelong disability.
Whether the jaundice is physiological or pathological should be identified and diagnosed by the physician. Physiological jaundice is always a diagnosis of exclusion; physiological or pathological, and under certain conditions, it can be transformed, and it is more risky to dispose of it by guessing and taking chances.
Causes
Bilirubin production is higher
1.Insufficient capacity of transfer bilirubin function
2.Poor uptake of unconjugated bilirubin by liver cells
3.Improper development of liver enzyme system
4, poor excretion of conjugated bilirubin
Jaundice symptoms
Appears 2~3 days after birth and peaks on the 4th~5th day; subsides within 2 weeks in full-term infants and extends to 3~4 weeks in preterm infants.
Early onset (most <24 hours); heavy; long duration; receding and reappearing or progressive aggravation.
Serum bilirubin
1. Total serum bilirubin <221 μmol/L in term infants and <256 μmol/L in preterm infants;
2.Serum bilirubin is mainly unconjugated bilirubin, conjugated bilirubin <34μmol/L;
3, daily rise <85μmol/L.
4.Serum total bilirubin >221~256μmol/, or reach the standard of phototherapy intervention under the corresponding day age and corresponding risk factors; or daily rise more than 85μmol/L;
5.Serum conjugated bilirubin >34μmol/L.
Systemic condition
Asymptomatic, in good general condition.
Symptomatic, varies with primary disease and condition.