Difference btw Physiological vs Pathological jaundice

In utero, the fetus lives in a state of relative hypoxia, with a paO2 of approximately 35mmHg (compared to 80mmHg for a healthy child or adult.) To maximize the oxygen carrying capacity of the blood, the fetus produces more red blood cells (RBCs) than the normal adult or child has, with a Hct of up to 60 being normal.

At birth, structural and functional changes take place which enable the fetus to breathe room air, bringing the baby's paO2 up to the normal child-adult range. Thus the excess RBCs are no longer needed for O2 carrying capacity, and they begin to break down. This is a normal, physiologic change that occurs at birth. The breakdown of these RBCs releases bilirubin into the blood stream. So a rise in bilirubin within 24-48 hours of life is normal. Bilirubin is excreted primarily via the stool. Once a newborn begins feedings and establishes a regular pattern of stooling, the bilirubin passes harmlessly out of his system.

If something causes an excessive number of RBCs to break down (such as ABO or Rh incompatibility, birth trauma or infection) or impairs the baby's ability to pass bilirubin out of the gi tract (npo, delayed stooling, meconium ileus) the bilirubin level can rise to dangerous levels, requiring treatment to prevent buildup in the brain, (kernicterus) which can cause brain damage and death.

In simplest terms . . .

physiologic jaundice occurs more than 24 hours after birth

pathologic jaundice occurs less than 24 hours after birth.

Physiological hyperbilirubinemia (jaundice is just a symptom) is a build-up of bilirubin due to the normal hemolyisis of red blood cells that were needed for fetal circulation before birth and discarded afterward. Normally, the liver processes the bilirubin and converts it to a form that can be excreted in stool. In a newborn, the immature liver is just ramping up to function on its own apart from mom. The imbalance of an overabundance of bilirubin to process and a liver that is not at top speed yet allows the yellow pigment from hemolyzed red cells to accumulate in the blood and give the skin and sclera (whites of the eyes) the yellow tone we call jaundice.

Pathological hyperbilirubinemia (notice the similarity to "pathology") is related to a condition other than normal newborn bilirubin being processed slowly by an immature liver. Such conditions include an incompatibility between the baby's and the mother's blood types, incompatibility of additional blood factors, or liver problems. There is actual pathology involved that might require more aggressive and lengthier intervention than physiological bilirubin problems.

Physiological jaundice coupled with risk factors--small baby, multiples, exclusive breastfeeding, poor feeding, Asian babies, large cephalohematoma, and a few others--can cause the serum bilirubin level to reach high risk levels and make the use of bili lights and blankets necessary. But generally speaking, pathological bilirubin levels reach higher levels sooner and take a longer time to come down.

Both conditions, if the numbers reach high enough levels, may require one or more exchange transfusions, although this is more likely with pathological jaundice.

If you Google any of these terms, include positive Coombs test as well, as this is what we sometimes see with pathological jaundice.