When a baby is born, they transition to life outside the womb, and their body begins to complete tasks that the mother’s body did for them while they were in utero. This is one of the most beautiful elements of life, the way a baby’s body is designed to become independent. The human body is complex and truly remarkable.
What is jaundice?
An example of such a process is when a baby’s body begins to break down red blood cells after they are used up. This system is important to understand at a basic level because problems can occur at various stages. This is how we determine the cause and treatment should an issue arise.
The cycle begins in the spleen; red blood cells are broken down into a byproduct of heme called bilirubin. It is bound to a protein called albumin in the bloodstream and transported into the liver, where it is conjugated (aka, made water-soluble, so it can ultimately be eliminated). Bilirubin then moves through the biliary tract and into the intestines. It is processed there with enzymes and gut bacteria.
Some of it returns to the liver, and the rest is passed out in the stool or enters the bloodstream, where it is then excreted to the kidneys and passed out in the urine. As a matter of fact, this is what gives urine its yellow color. When there is excess bilirubin in the blood, called hyperbilirubinemia, this leads to yellowing of the skin, which is called jaundice.
What are the different types of jaundice, and what causes them?
50-60% of all full-term babies have some degree of jaundice. It is even more common, approximately 80%, in babies that are born prematurely. Jaundice, contrary to popular belief, can actually be due to normal newborn conditions, which we call physiologic jaundice. Much less common, jaundice is found to be due to abnormal causes, called pathologic jaundice.
As a baby transitions from relying on the placenta to rid the body of excess bilirubin to their own body clearing it, many experience physiologic jaundice.
In the first few days of life, newborns produce more bilirubin because of greater production and faster breakdown of red blood cells. A newborn’s body is not always ready to deal with that extra bilirubin right away. The liver, which helps eliminate it, may be immature at birth, and the intestines are also not moving as fast early on. Together, this leads to a baby’s diminished ability to clear bilirubin. This is normal, temporary, and resolves with time. Visible physiologic jaundice usually appears on day 2 or 3 of life, peaks at day 4 or 5, and resolves by 1 to 2 weeks of age in a full-term baby.
After birth, breastfeeding moms provide colostrum as nutrition to the baby prior to mature milk. Breastfed babies may become jaundiced due to inadequate intake of breastmilk early on, termed breastfeeding jaundice. Additionally, there is a substance in breastmilk that actually blocks the removal of bilirubin; this may lead to breastmilk jaundice which presents on days 4-7 of life, lasts 3-12 weeks, and generally is not harmful.
There are other underlying disorders and conditions which may cause an infant to be jaundiced. In these cases, jaundice often appears much earlier or much later than does the more common form of infant jaundice. These are signs that jaundice in a newborn may be pathologic:
- Visible jaundice on the first day of life
- Bilirubin levels are rising fast
- Elevated conjugated bilirubin (>20% of total serum bilirubin)
- The level continues to rise after day 5
While rare and often treatable, pathological jaundice can be caused by any of the following:
- ABO incompatibility — An incompatibility between the mother’s blood and the baby’s blood. Mom may have antibodies that will cross the placenta and attack the baby’s red blood cells if they have different blood types.
- Rh incompatibility — a serious but rare condition where there is an attack on fetal red blood cells by maternal antibodies resulting in breakdown (hemolysis)
- Crigler-Najjar syndrome — a liver enzyme is missing or deficient, so the bilirubin can’t be conjugated, made into a form that can be eliminated from the body
- Dubin-Johnson syndrome — a defect (gene mutation) in the protein responsible for moving bilirubin into the biliary tract
- Biliary atresia — a condition with a defect in the biliary tract where the bile ducts are blocked or scarred (Treated with a surgery called a Kasai procedure)
- Neonatal hepatitis — a disease of the liver tissue due to an infection
- Hemorrhage — internal bleeding resulting in increased breakdown of red blood cells
- An infection in a baby’s blood (sepsis), other viral or bacterial infections
- Liver malfunction
- Enzyme deficiencies
- Abnormalities of a baby’s red blood cells that causes them to break down more rapidly
What tests are performed to screen for this?
- Pregnant women who are Rh-negative are checked for anti-Rh titers to determine if she needs Rh immunoglobulin administration during pregnancy.
- Physical exam (looking for yellowing of skin or yellowing of the whites of the eyes, called sclera icterus).
- All babies before discharge from the hospital undergo a screening skin test with a device called a transcutaneous bilirubinometer, which measures the reflection of a special light through their skin.
- Various laboratory blood tests of a baby, including total serum bilirubin, direct (conjugated) bilirubin, indirect bilirubin, a Direct Coomb’s test, and other tests as indicated.
What are the risk factors that make it more likely that a baby will have it?
- Premature birth — A baby born before 38 weeks of gestation may not be able to process bilirubin as quickly as full-term babies do. They may also feed less and have fewer bowel movements, resulting in less elimination through the stool.
- Significant bruising during birth — Newborns who become bruised during delivery may have higher bilirubin levels from the breakdown of more red blood cells.
- Blood type — As discussed above, if a mother’s and her baby’s blood types are different, the baby may receive antibodies through the placenta that cause rapid breakdown of red blood cells.
- Breastfeeding — Breastfed babies, particularly those with difficulty nursing, due to dehydration or low caloric intake.
- Heredity — Studies show that babies of East Asian ancestry have an increased risk of developing jaundice.
How is jaundice treated?
Mild infant jaundice often disappears on its own within two or three weeks. For moderate or severe jaundice, your baby may need to stay longer in the nursery or be readmitted to the hospital. The following are ways that we treat jaundice in newborns:
Your doctor may recommend more frequent feeding or supplementation to ensure that your baby receives adequate nutrition to prevent weight loss.
Light therapy (phototherapy)
Your baby may be placed under a special lamp that emits light in the blue-green spectrum. There may also be light provided via a bili-bed (pad or mattress) or a bili-blanket. The light changes the bilirubin molecule’s shape and structure so it can be excreted in the urine and stool. During treatment, your baby will wear protective eye patches.
Intravenous immunoglobulin (IVIG)
If jaundice is due to blood type incompatibility, an intravenous transfusion of an immunoglobulin — a blood protein that reduces antibody levels — may decrease jaundice and lessen the need for an exchange transfusion.
Rarely, when severe jaundice doesn’t respond to other treatments, a baby may need an exchange transfusion of blood. This involves repeatedly withdrawing small amounts of blood and replacing it with donor blood, diluting the bilirubin and maternal antibodies.
Why is jaundice important to recognize and treat?
Jaundice in most babies is mild and fully resolves without any long-term consequences. It is noteworthy, however, that serious complications can arise from leaving jaundice unmonitored or untreated. The level of bilirubin can increase to a point that is harmful, around 20 mg/dL.
While reaching a level this high is rare, it is important to monitor levels so that we intervene before it gets to these dangerous levels, as bilirubin is toxic to cells of the brain. There’s a risk of bilirubin passing into the brain, a condition called acute bilirubin encephalopathy. Signs of acute bilirubin encephalopathy in a baby include listlessness, difficulty waking, high-pitched crying, poor feeding, arching of the neck and body, fever, or kernicterus.
Kernicterus is the syndrome that occurs if acute bilirubin encephalopathy causes permanent damage to the brain. Kernicterus may result in involuntary and uncontrolled movements (athetoid cerebral palsy), permanent upward gaze, hearing loss, and improper development of tooth enamel.
The following signs or symptoms may indicate severe jaundice or complications from excess bilirubin. Call your doctor if:
- Your baby’s skin becomes more yellow, or the jaundice doesn’t improve or go away
- The skin on your baby’s abdomen, arms, or legs looks yellow
- The whites of your baby’s eyes look yellow
- Your baby appears sick, listless, or is difficult to wake
- Baby isn’t gaining weight or is feeding poorly
- Your baby makes high-pitched cries
- The stools are light gray or pale in color
Keep in mind that the likelihood of severe jaundice and the diseases described above are rare. However, this is why we as pediatricians monitor the bilirubin levels and have close follow up after birth! It is vital for your pediatrician to be aware of your baby’s feeding patterns, urine and stool output, and to visualize the baby’s skin over their entire unclothed body. Our role as your pediatrician is to think about and closely watch out for these things so that you, as new parents, don’t have to.