Jaundice is the most common medical condition observed in newborns, affecting a majority of full-term infants during their first week of life. This yellowing of the skin and eyes is a visible symptom of hyperbilirubinemia, which is an excess of the yellow pigment bilirubin in the blood. Bilirubin is a byproduct created when the body breaks down old red blood cells, a natural process that occurs constantly. Before birth, the mother’s liver processes this substance for the baby, but after delivery, the newborn’s system must take over. When the baby’s liver cannot process the bilirubin load quickly enough, the pigment accumulates in the bloodstream, leading to the characteristic yellow discoloration.
Defining the Differences in Timing and Bilirubin Levels
The distinction between the two types of newborn jaundice lies primarily in the timing of onset and the concentration of total serum bilirubin (TSB). Jaundice appearing within the first 24 hours after birth is always considered a sign of a pathological condition, requiring immediate medical evaluation. Conversely, jaundice that does not become visible until 48 to 72 hours after delivery is more likely to be the common, self-limiting physiological type. TSB is the measurement used to confirm and monitor the level of the pigment in the circulation.
A rapid rate of increase in bilirubin is a significant warning sign, with a rise greater than 5 milligrams per deciliter per day suggesting a pathological process. Physiological jaundice in a healthy, full-term baby typically peaks at a TSB level of about 5 to 6 mg/dL around the third or fourth day of life. A TSB concentration exceeding 17 mg/dL in a full-term newborn, or one that plots above the 95th percentile on age-specific nomograms, indicates a severe condition. These age-specific charts allow healthcare providers to assess the risk of severe hyperbilirubinemia.
Physiological Jaundice: Mechanism and Typical Course
Physiological jaundice is an expected biological process resulting from the newborn’s transition to independent life outside the womb. The mechanism involves two main factors: increased production of bilirubin and the temporary decrease in the liver’s ability to clear it. Neonates have a higher concentration of red blood cells, which also possess a shorter lifespan compared to those of an adult, leading to a significantly increased rate of red blood cell breakdown and bilirubin generation.
The newborn’s liver is functionally immature, particularly concerning the enzyme UGT (uridine diphospho-glucuronosyltransferase). This enzyme is responsible for converting fat-soluble, unconjugated bilirubin into a water-soluble, conjugated form that the body can excrete. The low activity of UGT means the liver is slow to process the high bilirubin load, causing it to build up in the blood.
This form of jaundice is generally transient, peaking around day three to five, and then progressively resolving within one to two weeks as the liver matures. Management is usually non-invasive, focusing on ensuring the baby receives adequate nutrition through frequent feeding. Adequate intake helps promote bowel movements, which is the primary way the body eliminates bilirubin. Supplementation with water or sugar water is avoided.
Pathological Jaundice: Identifying Underlying Causes and Treatment Needs
Pathological jaundice signals an underlying medical condition that is disrupting the normal processing or elimination of bilirubin, making it a more serious concern than the physiological type. One common cause is a blood group incompatibility, such as Rh or ABO incompatibility between the mother and baby, which triggers a rapid breakdown of the baby’s red blood cells, a process called hemolysis. Other underlying origins include infection, such as sepsis, or inherited red blood cell disorders like Glucose-6-Phosphate Dehydrogenase (G6PD) deficiency.
Structural problems in the liver or biliary system, such as biliary atresia, where the bile ducts are blocked or absent, can also cause pathological jaundice. This type may also present as a prolonged jaundice lasting more than two weeks, or as an elevation in the conjugated (direct) bilirubin level. Active medical intervention is necessary to prevent unconjugated bilirubin from reaching dangerously high levels that can penetrate the blood-brain barrier.
Untreated, severe hyperbilirubinemia can lead to a condition known as kernicterus, a form of brain damage caused by the pigment depositing in brain tissue. To lower the bilirubin concentration, the first-line treatment is phototherapy, where the baby is exposed to special blue light that changes the bilirubin molecule into a form easily excreted in the urine and stool.
In cases where the TSB level is dangerously high or rising despite phototherapy, an exchange transfusion may be performed, a procedure that involves removing small amounts of the baby’s blood and replacing it with donor blood. Intravenous Immunoglobulins (IVIG) may also be used when the jaundice is caused by immune-mediated red blood cell destruction.