2025 – PAGE 172 – NEONATOLOGY
RISK FACTORS FOR DEVELOPING HYPERBILIRUBINEMIA
Mild hyperbilirubinemia is common, but the risk factors for developing significant hyperbilirubinemia include sibling with history of phototherapy, bruising, cephalohematoma, Down syndrome, macrosomic infant of a diabetic mother, lower gestational age than 40 weeks, jaundice within 24 hours of birth, predischarge bilirubin close to the phototherapy threshold, and exclusive breastfeeding that is not going well. However, regarding the decision to use PHOTOTHERAPY to prevent neurotoxicity from severe hyperbilirubinemia, there are just FIVE NEUROTOXICITY RISK FACTORS to consider:
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- Gestational age < 38 weeks
- Albumin < 3 g/dL
- Isoimmune hemolytic disease (positive direct antiglobulin test), G6PD deficiency, or other hemolytic conditions
- Sepsis
- Significant clinical instability in the previous 24 hours
- PHOTOTHERAPY THRESHOLDS IF THERE ARE NO NEUROTOXICITY RISK FACTORS:
- PHOTOTHERAPY THRESHOLDS IF AT LEAST ONE NEUROTOXICITY RISK FACTOR IS PRESENT:
PEARL: NONE OF THE ABOVE-MENTIONED BILIRUBIN THRESHOLDS APPLY TO PREMATURE NEONATES < 35 WEEKS.
PEARL: If there is ANY concern that the child will develop hyperbilirubinemia, have the family follow up at 48 hours.
(DOUBLE TAKE) RHESUS DISEASE (AKA RH DISEASE)
When checking for Rhesus Disease (AKA RH Disease), look for an Rh- mom in her SECOND pregnancy: Maternal IgM antibodies are made during the FIRST pregnancy after exposure to the Rh antigen and are too large to cross over into the fetal circulation. During the SECOND pregnancy, IgG antibodies are present that are small enough to cross. (This can cause ERYTHROBLASTOSIS FETALIS if they cross early in pregnancy.) Rh- moms are supposed to get RHOGAM at 28 weeks gestation, and then again after delivery if the baby is found to be Rh+.
* KLEIHAUER BETKE TEST: Check MATERNAL blood to see if there are FETAL red cells present.
PEARL: RH disease is never present in a “first” pregnancy. ABO incompatibility can occur in ANY pregnancy.
(DOUBLE TAKE) ABO INCOMPATIBILITY
ABO incompatibility usually occurs in mothers with an “O” blood type. Naturally occurring “anti-A” or “anti-B” IgG antibodies may be present. This can result in hemolytic disease of the newborn in a FIRST pregnancy. So for hemolysis in a G1P1 baby, consider ABO incompatibility as the etiology.
MNEMONIC: In ABO incompatibility, mom is the one with the O blood type. mOm = mOm, AB = BAby.
(DOUBLE TAKE) GLUCOSE-6-PHOSPHATE DEHYDROGENASE DEFICIENCY (G6PD DEFICIENCY)
Glucose-6-Phosphate Dehydrogenase Deficiency (G6PD Deficiency) is an X-linked recessive disorder (so look for a male patient!) resulting in jaundice, dark urine, and anemia due to hemolysis from oxidative injury. In newborns, this can present with jaundice in a MALE baby within the first 24 HOURS of life. In other children, it can result in hemolysis after ingestion of fava beans, malaria medications, trimethoprim-sulfamethoxazole, ciprofloxacin, or nitrofurantoin. Look for HEINZ BODIES (purple granules noted in the red cells on microscopy). G6PD Deficiency is associated with patients of African American and Mediterranean descent.
PEARL: Do not test for the deficiency during the acute hemolytic phase. Instead, wait a few weeks because a false negative result can occur due to the build-up of G6PD in reticulocytes.
MNEMONIC: Imagine a bottle of HEINZ BODIES ketchup that has an X located on the exact spot that you have to hit it to make the broken RBCs come out of the bottle. Or, look at this X-shaped HEINZ BODIES bottle of ketchup.
NAME ALERT: This is not the same as glucose-6-phosphatase deficiency, which can affect glucose metabolism and is associated with glycogen storage disease 1, von Gierke’s disease.