Cf Peds Ch19 Neonatal Hyperbilirubinemia

Front 1

1. What does Neonatal hyperbilirubinemia result from?

Back 1

a. Higher rates of bilirubin production and limited ability to excrete it.
b. It includes physiologic jaundice and non-physiologic jaundice.
c. The infant has several risk factors for neonatal physiologic jaundice.
d. Male gender, cephalohematoma, Asian origin, and breast-feeding

Front 2

2. Other possible risk factors for neonatal hyperbilirubinemia?

Back 2

a. Maternal diabetes
b. Prematurity Polycythemia
c. Trisomy 21
d. Cutaneous bruising
e. Delayed bowel movement
f. Upper gastrointestinal obstruction
g. Hypothyroidism
h. Swallowed maternal blood
i. Sibling w/physiologic jaundice

Front 3

3. What conditions can cause non-physiologic jaundice when excessive unconjugated bilirubin accumulates?

Back 3

a. RBCs are lysed at too rapid a rate
b. Transmission of unconjugated bilirubin to the liver is interrupted
c. Liver enzyme deficiencies preclude appropriate metabolism of the unconjugated material.

Front 4

4. Risk of hyperbilirubinemia?

Back 4

a. Untreated severe Unconjugated hyperbilirubinemia is potentially neurotoxic.

Front 5

5. Conjugated (Direct) Bilirubin?

Back 5

a. Bilirubin chemically attached to a glucuronide by an enzymatic process in the liver.

Front 6

6. Erythroblastosis Fetalis?

Back 6

a. Increased RBC destruction due to transplacental maternal antibody passage active against the infant’s RBC antigens.

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7. Kernicterus?

Back 7

a. A neurologic syndrome resulting from unconjugated bilirubin deposition in brain cells, especially the basal ganglia, globus pallidus, putamen, and caudate nuclei.
b. Less mature or sick infants have greater susceptibility.
c. Lethargy, poor feeding, and loss of Moro reflex are common initial signs.

Front 8

8. Polycythemia definition?

Back 8

a. A central hematocrit of 65% of higher, which can lead to blood hyperviscosity.

Front 9

9. Unconjugated (indirect) bilirubin?

Back 9

a. Bilirubin yet to be enzymatically attached to a glucuronide in the liver.

Front 10

10. Physiologic jaundice?

Back 10

a. Comprises primarily unconjugated hyperbilirubinemia observed during the first week of life in approximately 60% of full-term infants and 80% of preterm infants.
b. Full-term newborns usually have a peak bilirubin concentration of 5-6 between the second and fourth days of life!

Front 11

11. Findings suggestive of non-physiologic jaundice?

Back 11

1. Appearance in the first 24-36 hours.
2. Bilirubin rate of rise > 5mg/dl/24 h.
3. Bilirubin >12 mg/dl in a full-term infant w/o other physiologic jaundice risk factors listed.
4. Jaundice that persists after 10-14 days of life.

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12. Causes of non-physiologic jaundice?

Back 12

1. Septicemia
2. Biliary atresia
3. Hepatitis
4. Galactosemia
5. Hypothyroidism
6. Cystic Fibrosis
7. Congenital haemolytic anaemia (eg spherocytosis, maternal Rh or blood type sensitization)
8. Drug-induced haemolytic anaemia.

Front 13

13. Causes of jaundice presenting w/I the first 24 hours of life? (requires immediate attention)

Back 13

1. Erythroblastosis fetalis
2. Haemorrhage
3. Sepsis
4. Cytomegalic inclusion disease
5. Rubella
6. Congenital toxo

Front 14

14. What neuro condition can unconjugated bilirubin cause?

Back 14

a. Kernicterus, the signs of which mimic sepsis, asphyxia, hypoglycemia, and intracranial haemorrhage.

Front 15

15. Common initial signs of kernicterus?

Back 15

a. Lethargy and poor feeding.

Front 16

16. Breast-milk jaundice?

Back 16

a. ~2% of breast-fed full-term infants develop significant unconjugated bilirubin elevations (breast-milk jaundice) after the 7th day of life.
b. Concentrations up to 30 mg/dL during the 2nd to 3rd week of life can be seen!

Front 17

17. Tx of breast-milk jaundice?

Back 17

a. If continued, the levels gradually decrease.
b. If switched to formula for 12-24 hours, there is rapid bilirubin level decrease.
c. Breast-feeding can be resumed w/o return to hyperbilirubinemia.

Front 18

18. Monitoring of full-term, low-risk but jaundiced infants?

Back 18

a. Monitored with Serum bilirubin levels.
b. Significant levels require a diagnostic evaluation, including indirect and direct concentration, hb level, retic count, blood type, Coombs, .

Front 19

19. What does indirect Coombs measure?

Back 19

a. Antibodies to RBCs in the blood.

Front 20

20. What does direct Coombs measure?

Back 20

a. Identifies antibodies on the infant’s RBCs.

Front 21

21. Alternative to measuring serum bili?

Back 21

a. Non-invasive, transcutaneous measurement using multi—wavelength spectral reflectance.

Front 22

22. Tx of physiologic jaundice (unconjugated hyperbilirubinemia)?

Back 22

a. Phototherapy: the unclothed infant is placed under a bank of lights, eyes shielded, and hydration maintained.
1. The light changes the skin’s bilirubin isomerization into an extractible form.
2. For full-term infants w/o haemolysis, phototherapy is initiated at the following levels: 16-18 at 24-48 hours, 16-18 at 49-72 hours, and ≥ 20 mg/dl at 72 hours.
b. Exchange transfusion is needed in a small number of jaundiced infants who do not respond to conservative measures.

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23. What drug, given to the mother during pregnancy reduces neonatal jaundice?

Back 23

a. Phenobarbital, which induces glucuronyl transferase

Front 24

24. How do sepsis and acidosis increase to risk of neurologic damage from bilirubin?

Back 24

a. By increasing the blood-brain barrier’s permeability to bilirubin.

Front 25

25. How would Gilbert syndrome present in terms of Coombs test, hemoglobin, retic count, and bili?

Back 25

a. Negative Coombs
b. Normal (or low) hemoglobin
c. Normal (or slightly elevated) retic count
d. Prolonged hyperbilirubinemia.

Front 26

26. In what 2 conditions would red cell morphology be abnormal?

Back 26

a. DIC and spherocytosis.

Front 27

27. Coombs w/a blood group isoimmunization?

Back 27

a. Positive Coombs test

Front 28

28. What liver enzyme are all infants relatively deficient in?

Back 28

a. Uridine diphosphate glucuronosyltransferase.

Front 29

29. What condition has severe deficiency of Uridine diphosphate glucuronosyltransferase?

Back 29

a. Crigler-Najjar Type 1.
b. Causes high bilirubin levels and encephalopathy

Front 30

30. Tx of Crigler-Najjar type 1?

Back 30

a. Phototherapy? Double check this. Somewhere else

Front 31

31. Bili in Crigler-Najjar type I?

Back 31

a. Rarely exceed 20.
b. Encephalopathy is rare.