The term jaundice refers to a yellow discoloring of the skin and the sclera (the white part of the eyes). Jaundice in the newborn is called neonatal jaundice, and it may develop for a variety of reasons. Before taking a look at those reasons, let’s first discuss jaundice as a phenomenon occurring in anybody.
Whether in the skin, where it is most notable, or in the sclera, jaundice is a yellowing that develops because of an excess of a pigment called bilirubin circulating through the body. Bilirubin is produced when a chemical called heme is broken down. In body cells, heme is connected to a handful of different proteins and enables them to do their jobs. The largest source of heme is hemoglobin, the protein that carries oxygen in red blood cells (RBCs). When RBCs get too old to work well, or when they are abnormal, they break down. Their hemoglobin gets stripped of its heme component, which is converted to bilirubin, specifically a type of bilirubin called unconjugated, or indirect bilirubin. Released into the bloodstream, unconjugated bilirubin binds to a protein called albumin and travels that way to the liver, where it is released from the albumin and transformed into conjugated bilirubin. Also called direct bilirubin, conjugated bilirubin is bilirubin that is attached to a molecule called glucuronate. Conjugation to glucuronate enables the bilirubin to dissolve in water, allowing it either to be excreted from the liver as part of a dark-green to yellow fluid called bile, or to reenter the bloodstream and be excreted into the urine by the kidneys. Released into the small intestine and also stored in the gallbladder, bile aids in the digestion of food by breaking down fat. It is normal to have some bilirubin circulating in the blood, but jaundice results when the concentration of bilirubin rises and it can happen from an increase in conjugated (direct) bilirubin, unconjugated (indirect) bilirubin, or both.
As for the causes of jaundice in the neonate, the most common cause is known as physiological jaundice, meaning jaundice resulting from normal body processes as opposed to abnormalities. Not only do fetuses and newborns have a very high concentration of RBCs and hemoglobin compared to adults, their RBCs are more fragile than yours are so they break apart easily, releasing indirect bilirubin. On top of that, the liver in fetal and neonatal life is not functioning yet at full speed so it conjugates bilirubin relatively slowly. Now, during fetal life, the placenta —the organ connecting the mother to the fetus by way of the umbilical cord— normally removes the fetal bilirubin, but the connection with the placenta is cut at birth, leaving bilirubin from broken RBCs to accumulate to higher concentrations. This causes a mild rise in the level of bilirubin shortly after birth with mild jaundice developing usually between 2 to 7 days after birth. Normally, this resolves within 10 days without treatment. In a process called umbilical cord milking, obstetricians commonly used to squeeze the umbilical cord prior to clamping it off from the newborn, and still do it in cases of premature birth when judging that the newborn could use more blood volume. However, some research suggests that this practice may cause a condition called neonatal polycythemia in which there are too many RBCs and also cause neonatal jaundice.
As for treatment of neonatal jaundice, this depends on the severity of the baby’s elevated bilirubin levels and the underlying cause. Generally, the less mature the newborn at birth, the more serious the condition.
Other causes of neonatal jaundice result from problems either causing excessive production of bilirubin or decreased clearance (removal) of bilirubin. Conditions causing increased production of bilirubin include hemolytic disease of the newborn (newborn RBCs breaking apart excessively), hemorrhage (severe bleeding) including in the brain, polycythemia (too many RBCS, resulting from overproduction of RBCs rather than from cord milking), sepsis (infection throughout the body), disseminated intravascular coagulation (a severe disorder of the blood clotting system), and G6PD deficiency (a genetic enzyme disorder that causes RBCs to break). Conditions causing decreased clearance of bilirubin include prematurity (because the liver is not working up to full speed), breast milk jaundice, neonatal cholestasis (a liver disease), extrahepatic biliary atresia (lack of the duct that normally carries bile to the small intestine), hormonal problems such as low levels of thyroid or pituitary hormones, and a genetic condition called Gilbert syndrome.
Explaining every one of these conditions would go beyond the scope of this post, so let’s focus on just a couple that are fairly common. Hemolytic disease of the newborn happens on account of the mother’s immune system making antibodies against special molecules that exist on the surface of the baby’s RBCs. We have discussed this condition here on The Pulse, and it can happen as a result of incompatibility between the ABO blood type of the mother and baby and especially as a result of incompatibility between the mother and baby of what is called the D antigen of the Rhesus (Rh) blood group system typing. This happens when the mother is Rh-negative and her baby is Rh-positive and usually it does not happen during the first pregnancy of an Rh-negative mother with an Rh-positive baby, but during and after subsequent pregnancies. Knowing the mother’s blood type, the situation can be prevented if the mother takes an antibody medication called RhoGAM.
Being premature can lead to jaundice, and we have listed it above with the clearance problems on account of the liver. Essentially, it happens from the same reason as physiological jaundice, but the process is exaggerated because the liver of a premature newborn is less active than the liver of a baby who is born at term. It is very important to treat such newborns because continued presence of high levels of bilirubin can damage the brain.
Breast milk jaundice is jaundice that strikes the nursing newborn on account of substances in the breast milk that interfere with the liver’s ability to process the bilirubin. So, while there are many advantages to breastfeeding, the potential for breast milk jaundice is one disadvantage, as the the infant formulas that are given to babies that are not breastfed do not contain such substances.
Although fairly rare, neonatal sepsis, an infection throughout the body, is a very serious condition that needs to be recognized early so it can be treated with antibiotics, but one clue to possible sepsis is jaundice developing within 24 hours of birth.
As for treatment of neonatal jaundice, this depends on the severity of the baby’s elevated bilirubin levels and the underlying cause. Generally, the less mature the newborn at birth, the more serious the condition. Infants with mild jaundice who are born after the 35th week, often do not need any treatment other than good nutrition. Otherwise, the majority of cases are treated with phototherapy in which light in the blue-green range is shined all around the baby, whose eyes are covered to prevent eye damage. This light accelerates the breakdown of bilirubin. Certain cases must be treated with intravenous immunoglobulin (IVIG). Very severe cases may need exchange transfusion, in which portions of the newborn’s blood are removed while donated blood is transfused in, causing bilirubin to get diluted along with any antibodies from the mother that might be causing the condition.