This next entry deals with hyperbilirubinemia and jaundice in the late preterm infant. Just to recap, late preterm as defined by AWHONN is an infant born between 34 and 36 completed weeks' gestation.
During the antenatal period, fetal hemoglobin levels are necessarily higher than postnatal. Increased hemoglobin is needed to carry oxygen from the maternal/placental blood into fetal tissue for the massive perfusion and growth needed in the third trimester of pregnancy. Fetal hemoglobin levels tend to decrease as the 40-week mark of pregnancy approaches, since fetal brain and tissue growth needs decline.
At birth and shortly thereafter, fetal hemoglobin levels begin to drop dramatically, as the newborn is now sufficiently self-oxygenating via respiration. Since fetal hemoglobin is no longer necessary such large quantites, a portion of the erythrocytes carring it begin to hemolyze. This hemolysis causes bilirubin - also contained therein - to spill into circulation. The liver then conjugates the bilirubin for excretion.
For normal newborns, whose fetal hemoglobin has already begun to decrease, and who tend to eat well and stool regularly (the body's method of bilirubin excretion), this is generally not a problem, even when the infant's skin takes on the yellow-orange coloring we call jaundice.
For the late preterm infant, however, the story changes a bit. Their fetal hemoglobin levels are generally higher to begin with, leaving more erythrocytes to hemolyze. Their livers are not as fully developed as a full-term newborns. So the double whammy of too much bilirubin plus not as much liver maturity to excrete becomes a recipe for hyperbilirubinemia/jaundice in late pretermers.
Why is this a problem? Well, for starters the late pretermer brain is less fully developed than the full-term newborn brain. There is a tremendous amount of brain growth and development in the last four to six weeks of pregnancy. Thus, it stands to reason that the brain of a late pretermer would be less resilient to insult than that of a full-termer. Extreme hyperbilirubinemia can lead to kernicterus, an severe form of bilirubin-related brain damage. The preterm brain is more susceptible to this.
Additionally, preterm infants do not always have adequate intake related to their uncoordinated suck, whether breast or bottle-feeding. They tend to tire more easily while feeding as well. Both these situations can lead to a) dehydration; and b) poor stool output. As stooling is the body's major method of bilirubin excretion, decreased stooling leads to increased bilirubin.
So, what do we do with these kids? We do all we can do make sure they are eating and stooling properly to begin with. This goes a very long way in preventing bilirubin so elevated that it becomes problematic. All our preterm babies get a serum bilirubin drawn on their second day of life along with their metabolic screening. Our practitioners use a standardized normogram to decide if the serum bilirubin level warrants phototherapy. We are more aggressive in phototherapy for late pretermers than we would be for a fulltermer. Our pretermers with high bilirubin are often started out on double phototherapy in order to decrease it more rapidly, as there is less proverbial 'wiggle room' in treating these kids.
In the most extreme cases, the baby gets sent to intensive care for IV fluids, and possibly exchange transfusion. This is our last resort. Very fortunately, however, when we do all the aforementioned things, we do not have to use our last resort very often, and I daresay hyperbilirubinemia does not have nearly the mortality and morbidity it did a generation or two ago.
Some additional resources and information: