Baby's facial color changes when jaundice is gone

When babies are just born, they will have jaundice, with yellow skin, especially the face. But this phenomenon is normal. When the baby reaches a certain age, the jaundice will disappear naturally. Of course, there are individual cases. For example, some newborns have severe jaundice. This problem needs to be solved by a doctor. But what will happen to your baby’s facial complexion when the jaundice is gone?

Neonatal jaundice refers to a disease characterized by yellowing of the skin, mucous membranes and sclera due to accumulation of bilirubin in the body during the neonatal period (from the time the umbilical cord is tied after delivery of the fetus to 28 days after birth). The disease is divided into physiological jaundice and pathological jaundice. Physiological jaundice in full-term infants appears 2 to 3 days after birth, reaches a peak on the 4th to 5th day, and disappears on the 5th to 7th day, no later than two weeks; it lasts longer in premature infants, and except for mild loss of appetite, there are generally no other clinical symptoms. If jaundice appears within 24 hours after birth, does not subside within 2 to 3 weeks, or even continues to deepen and worsen, or reappears after subsiding, or jaundice begins to appear 2 weeks after birth, it is pathological jaundice. When the total serum bilirubin level in full-term infants exceeds 205.2 μmol/L (12 mg/dl) and that in premature infants exceeds 256.5 μmol/L (15 mg/dl), it is called hyperbilirubinemia, which is pathological jaundice. If the indirect bilirubin level in full-term infants exceeds 307.8 μmol/L (18 mg/dl), the chance of developing bilirubin encephalopathy (kernicterus) is high, which can damage the central nervous system and easily leave sequelae.

1. Excessive production of bilirubin

Due to excessive destruction of red blood cells and increased enterohepatic circulation, serum unconjugated bilirubin increases. Common causes include: polycythemia, extravascular hemolysis, alloimmune hemolysis, infection, increased enterohepatic circulation, erythrocyte enzyme deficiency, abnormal erythrocyte morphology, and hemoglobinopathy.

2. Hepatic bilirubin metabolism disorder

Due to the low function of liver cells to absorb and bind bilirubin, the serum unconjugated bilirubin increases. Common causes include: hypoxia and infection, Crigler-Najjar syndrome, Gilbert syndrome, Lucey-Driscoll syndrome, and drugs (such as sulfonamides, salicylates, indomethacin, and scutellariae).

3. Bile excretion disorder

Impairment in the excretion of conjugated bilirubin by hepatocytes or obstruction of the bile duct can lead to hyperconjugated bilirubinemia, but if accompanied by impaired hepatocyte function, unconjugated bilirubin may also increase. Common causes include: neonatal hepatitis, congenital metabolic defects, syndrome, and bile duct obstruction.

1. Bilirubin test

It is an important indicator for the diagnosis of neonatal jaundice. The serum bilirubin concentration (TSB) can be measured by venous blood or micro-blood method. The transcutaneous bilirubin meter is a non-invasive detection method with easy operation. The transcutaneous bilirubin value (TcB) is well correlated with the micro-blood bilirubin value. Since this method is affected by the thickness of the skin and skin color at the measurement site, it may mislead the jaundice situation. It can be used for screening. Once a certain limit value is reached, serum bilirubin needs to be tested.

2. Other auxiliary examinations

(1) Red blood cells, hemoglobin, reticulocytes, and nucleated red blood cells must be routinely checked when neonates have jaundice, which helps screen for hemolytic disease of the newborn. In the presence of hemolytic disease, the red blood cell count and hemoglobin decrease, and the reticulocytes increase.

(2) Blood type includes the blood types of the father, mother and newborn (ABO and Rh systems), which is very important, especially when neonatal hemolytic disease is suspected. If necessary, further serum specific antibody testing can be performed to assist in diagnosis.

(3) Red blood cell fragility test: This test can be performed if jaundice is suspected to be caused by hemolysis but hemolytic disease due to blood type incompatibility has been ruled out. If fragility increases, consider hereditary spherocytosis, autoimmune hemolytic disease, etc. If fragility is reduced, it can be seen in hemoglobin disorders such as thalassemia.

(4) The normal methemoglobin reduction rate is >75%. This value is lower in patients with G-6PD deficiency, and further G-6PD activity measurement is required to confirm the diagnosis.

(5) Blood, urine, cerebrospinal fluid culture, serum specific antibodies, C-reactive protein and erythrocyte sedimentation rate examination If jaundice is suspected to be caused by infection, blood, urine, cerebrospinal fluid culture, serum specific antibodies, C-reactive protein and erythrocyte sedimentation rate examination should be performed. The white blood cell count in the blood routine test is increased or decreased, with toxic granules and nuclear left shift.

(6) Liver function tests measure total bilirubin and conjugated bilirubin in the blood. Alanine aminotransferase is a more sensitive method to reflect liver cell damage. Alkaline phosphatase can be elevated in cases of intrahepatic bile duct obstruction or inflammation.

(7) Abdominal ultrasound is a non-invasive diagnostic technique, especially suitable for newborns. Diseases of the biliary system, such as bile duct cysts, bile duct dilatation, gallstones, biliary atresia, and gallbladder absence, can all show the pathological conditions.

(8) Electrophysiological examinations of auditory and visual functions, including brainstem auditory evoked potentials (BAEP), can be used to evaluate the functional status of auditory conduction nerve pathways, early predict brain damage caused by bilirubin toxicity, and assist in the diagnosis of temporary or subclinical bilirubin neurotoxicity.

The latest research shows that jaundice on the skin and eyes of newborns after birth has a protective effect on the body, which can protect it from damage by free radicals. All infants and adults have a protective mechanism against free radicals in their bodies. The latest research suggests that bilirubin in infants has a protective effect against them. This pigment is an antioxidant that causes newborns to show mild jaundice. Mild jaundice in newborns is physiological, but the high level of bilirubin in the body after birth should be taken seriously, and attention should be paid to whether there are pathological conditions. Bilirubin is caused by the breakdown of aging red blood cells and hemoglobin-containing components in the body. When the bilirubin accumulated in the blood exceeds the amount excreted by the liver into the intestines, jaundice occurs. It is well known that excessive bilirubin is harmful to infants, but the cause of mild increase in bilirubin after birth is still unclear. The bilirubin level in the blood of healthy infants can rise to 15-20 mg/dl one week after birth, but severe jaundice (bilirubin>25-30 mg/dl) will cause brain damage if not treated. Treatment of severe jaundice may include phototherapy, in which exposure to blue light changes bilirubin into a complex that is more easily excreted in the urine.

To understand the cause of the mild increase in bilirubin after birth, Dr. Snyder and his colleagues used in vitro experiments to block the enzyme that produces bilirubin and exposed the group of cells to a free radical environment. The results showed that cells without bilirubin were damaged and died, while cells that could produce bilirubin could still survive and pass on under the action of free radicals. Bilirubin circulates in the body and is an effective anti-free radical agent. As for why infants have higher bilirubin levels than adults, it may be related to the fact that newborns need to adapt to greater changes in the external environment. Previous studies have also suggested that adequate levels of bilirubin can reduce stroke, cancer and