Final answer:
The most common risk factor for developing severe hyperbilirubinemia in newborns is the immaturity of hepatic enzymes required to process bilirubin and meconium retention, which leads to increased bilirubin levels that can cause kernicterus and brain damage if not properly managed.
Step-by-step explanation:
The most common risk factor for developing severe hyperbilirubinemia in the newborn is immature hepatic enzyme systems which fail to adequately conjugate bilirubin and meconium retention which hinders the clearance of bilirubin. In neonates, bilirubin is derived from the breakdown of erythrocytes and is typically processed by the liver and secreted in bile. This enter-hepatic circulation is critical in the first days of a newborn's life, as meconium clearance aids in bilirubin excretion. Unconjugated hyperbilirubinemia occurs when the enzyme UDP glucuronyl transferase is not fully developed, leading to the accumulation of bilirubin in the blood. Excessive levels of unconjugated bilirubin can exceed the binding capacity of albumin and penetrate the blood-brain barrier, potentially causing kernicterus and neurotoxicity.
Newborn jaundice is a common condition linked to high levels of bilirubin. It's crucial that bilirubin levels are monitored and kept low to prevent the risk of brain damage due to its neurotoxic effects. Breastfeeding and the expelling of meconium are natural processes that help prevent hyperbilirubinemia by promoting the excretion of bilirubin. If the levels become high, newborns may receive phototherapy to help break down the bilirubin more rapidly, reducing the risk of kernicterus.