The tendency for newborns to turn yellow in the days after birth has been observed for centuries.
In Korea, the days after birth are called “Huang Dal” or “yellow-time” and accepted as a normal phase of newborn life.
Bilirubin is the chemical that makes baby’s skin turn yellow. Babies are born with extra red blood cells, and as the cells are broken down, the left over hemoglobin pigment is converted into bilirubin.
The bilirubin is then excreted by the kidneys and liver, which is why urine is yellow and stool is brown.
The liver step involves enzymes which allow the bilirubin to get into bile and then to the intestinal tract.
The first stools of newborns – called meconium – are tarry and black because they’re mostly composed of fetal bile.
Adults produce bilirubin, but are more adept at excreting it. Newborn liver function is immature in the days after birth, leading to elevation in bilirubin and jaundice in most newborns.
Premature babies are not only more immature in their handling of bilirubin they are also more sensitive to its toxic effects.
Additionally, genetic variants that impair bilirubin metabolism are common.
Five to 10 percent of babies have an enzyme mutation called Gilbert’s disease that often leads to jaundice.
More than 40 percent of Asian babies have mutations in these enzymes, and interestingly, many African-American infants have the opposite: a supercharged enzyme that leads to much lower bilirubin values in infancy.
In addition to liver immaturity, newborns are in a semi-starvation mode at birth; breast milk is not abundant for the first few days after birth.
Babies all lose weight and are a little on the dry side as they await mother’s plentiful milk on day 2 to 4 of life. The bile-laden meconium sits in their GI tract and the bilirubin is reabsorbed from the gut.
The hydration that comes after the newborn starts to take in larger amounts of milk results in elimination of the meconium, and rapid maturation of liver enzymes leads most newborns to quickly clear their bilirubin load and jaundice within a week or so after birth.
Birth is a difficult process and many babies have bruising or hematomas on their scalp. This leads to extra red blood cell breakdown that adds to baby’s bilirubin burden.
Other infants have blood group differences from their mother that can lead to break down of blood cells – called hemolysis – and overwhelm their capacity to eliminate bilirubin.
The most severe hemolysis is that from Rh incompatibility, when the fetus becomes severely anemic from maternal antibodies to baby’s blood.
After birth, the baby can become terribly jaundiced. Fortunately, these days mothers receive an injection to prevent the antibodies from being produced and the incidence of Rh-sensitized mothers is much lower than in the past.
A milder form of hemolysis can happen when mother is blood type O and baby is A or B (like dad). This hemolysis is less severe and leads to jaundice needing treatment in only 15 percent of these babies.
Lastly, other genes that can cause hemolysis in newborns are common. G6PD is present in 13 percent of African American boys (the gene is on the X chromosome so males are most frequently affected), 5 percent of Asian and 5 percent of Mediterranean male infants. These babies can have mild to severe hemolysis and may require therapy.
We frequently see breast-fed babies with a combination of increased levels of bilirubin and poor bilirubin excretion that need some observation or treatment before they are safe to go home from the hospital.
Many cultures practice daily sun bathing for babies in the first weeks of life as a form of treatment. It wasn’t until 1956 when a British nurse noted that babies in the nursery near the windows were less jaundiced than those in the interior of the nursery.
Soon babies in South America and Europe were getting phototherapy to treat jaundice, but skeptical American physicians did not adopt the practice until 1968 when it was introduced by Dr. Jerold Lucey.
We now know that specific wavelengths of blue light make a molecular change in the bilirubin molecule that allows it to bypass the liver enzyme step and be easily excreted.
Today, many types of lights are available and are used in hospitals or at home to treat jaundiced babies.
Sunlight is a very potent form of phototherapy, but may put baby at risk for sunburn or hypothermia and so is not widely used in the United States.
Bilirubin is a potent antioxidant and serves a protective role in the body, but extremely high levels in newborns can have a catastrophic side effect. Certain parts of the newborn brain are sensitive to toxic effects of bilirubin, especially if baby is sick or premature.
If this occurs, the brain may be stained yellow in the central areas, called kernicterus. Babies that develop kernicterus may have permanent neurologic injury. They are cognitively normal, but have a form of spastic cerebral palsy, deafness and lifelong disability.
Doctors and nurses who care for newborns are very careful to assess each newborn for jaundice, feeding abilities, hydration and other risk factors for high bilirubin before babies are sent home.
About 8 percent of healthy, full-term newborns stay an extra day or two in the hospital for phototherapy to be sure that the baby has a safe experience with jaundice.
Parents are taught to watch for jaundice in their baby in the week after birth and are encouraged to take their baby in for a doctor check up in one to three days following discharge from the hospital.
Most visible jaundice starts on the head and moves down the body as the bilirubin level rises.
If the baby looks really yellow, jaundice is visible on the arms and legs or baby isn’t eating well, parents need to call the physician for an examination or take the baby to the emergency room.
It’s important to remember that most jaundice is a normal part of babyhood.
Babies with mild jaundice who are feeding well, making plenty of wet and dirty diapers and with good pediatric follow-up are sent home after just a day or two in the hospital and do just fine with no special treatment.