3. Neonatal Jaundice Flashcards
1
Q
True or False
Conjugated hyperbilirubinemia is always pathologic
A
True
Conjugated hyperbilirubinemia (when \> 20% of the total bilirubin is conjugated) is always pathologic and must be investigated further.
2
Q
Describe the physiology of bilirubin (4)
A
- Bilirubin is produced by the catabolism of hemoglobin.
- The initial breakdown product of hemoglobin is unconjugated bilirubin, which is not water soluble, and therefore must be made into a soluble product before it can be excreted.
- It is transported to the liver where the enzyme UDP-GT facilitates the conjugation of bilirubin.
- Conjugated bilirubin is water soluble, and is further broken down into urobilinogen and stercobilinogen, which are excreted in the stool and, to a lesser degree, in the urine.
3
Q
Name causes of Unconjugated Hyperbilirubinemia (3)
A
- Increased Production
- Decreased Conjugation (UDP-GT Deficiency)
- Increased Reuptake (via Enterohepatic Circulation)
4
Q
Name causes: Increased Production Unconjugated Hyperbilirubinemia (4)
A
- Extravascular blood (cephalohematoma)
- Polycythemia (delayed cord clamping, twin-to-twin transfusion)
- Red cell instability (G6PD, spherocytosis, elliptocytosis, decreased RBC half-life)
- Coombs positive: isoimmunization (Rh, ABO, minor antigens)
5
Q
Name causes: Decreased Conjugation (UDP-GT Deficiency) Unconjugated Hyperbilirubinemia (4)
A
- Prematurity
- Gilbert syndrome
- Crigler-Najjar syndrome
- Congenital hypothyroidism
6
Q
Name causes: Increased Reuptake (via Enterohepatic Circulation) of Unconjugated Hyperbilirubinemia (2)
A
- Breast-feeding jaundice (secondary to dehydration)
- Bowel obstruction (meconium ileus, etc.)
7
Q
Name causes of Conjugated Hyperbilirubinemia (3)
A
- Sepsis
- Intrauterine Infection (TORCH)
- Hepatic
8
Q
Name Intrauterine Infection causes of Conjugated Hyperbilirubinemia (5)
A
- Toxoplasmosis
- Other: syphilis, EBV
- Rubella
- Cytomegalovirus
- Herpes, HIV
9
Q
Name hepatic causes of Conjugated Hyperbilirubinemia (9)
A
- Biliary atresia
- Alagille syndrome
- Disorders of bile acid metabolism
- Neonatal hepatitis
- Choledochal cyst
- Underlying metabolic condition (Galactosemia, tyrosinemia)
- Infiltrative (Wilsons, a 1-antitrypsin deficiency)
- TPN -related cholestasis
- Cystic fibrosis
10
Q
Describe: Kernicterus (2)
A
- the neurologic outcome of bilirubin deposition in the basal ganglia and brainstem nuclei.
- It is a result of elevated unconjugated hyperbilirubinemia.
11
Q
Name signs: Kernicterus (9)
A
- Early signs:
- lethargy
- poor suck
- hypotonia
- high-pitched cry
- seizures
- Late signs:
- irritability
- hypertonia
- opisthotonos: is a state of severe hyperextension and spasticity in which an individual’s head, neck and spinal column enter into a complete “bridging” or “arching” position.
- fever
12
Q
Name Risk Factors for Severe Hyperbilirubinemia (8)
A
- Jaundice within the first 24 h of life
- Blood group incompatibility (DAT positive)
- Late preterm infants (35–36+ 6wk gestational age)
- Cephalohematoma
- Sibling requiring phototherapy
- Exclusively breast-feeding
- East Asian race
- G6PD deficiency
13
Q
Name: Rskfactors or Neonatal Sepsis (5)
A
- Rupture of membranes for >18h before delivery
- Maternal fever (T > 38°C) during labor
- Chorioamnionitis
- Maternal GBS colonization (i.e., GBS UTI)
- Prior delivery of an infant with GBS disease
14
Q
Describe HX: Neonatal Jaundice (5)
A
- Exact time and date of birth (to calculate the newborn’s age in hours)
- Onset, duration, progression, rate of change
- Pregnancy and delivery Hx: maternal illness (Hx of GBS UTI), blood type (maternal and newborn, if known), prenatal serologies, substance use during pregnancy, prolonged rupture of membranes, presence of maternal fever during delivery, if antibiotics were given during delivery (what type and how many doses), traumatic birth (presence of extravascular blood), delayed cord clamping, Apgar scores, gestational age, BW, bilirubin at time of discharge from hospital
- Postnatal Hx: breast-feeding versus formula feeding, frequency and length of feeds, presence of adequate milk supply if breast-feeding exclusively, number of wet diapers, pale stools or dark urine, waking to feed, medications/supplements, current weight (percentage weight loss from birth)
- FHx: pedigree, jaundice (scleral icterus), hematologic or metabolic disorders, anemia, liver disease, autoimmune conditions, ethnicity, early neonatal deaths, consanguinity
15
Q
Describe physical exam: Neonatal Jaundice (8)
A
- Vital signs: fever, tachycardia, level of consciousness
- Growth parameters: weight change from BW
- General inspection: cephalocaudal progression of jaundice, presence of hematomas
- Head: bulging versus sunken fontanelle, alert versus lethargic, scleral icterus
- Hydration status: mucous membranes, femoral pulses, capillary refill time
- Abdo: hepatosplenomegaly, ascites, dark urine, pale stools
- Skin: purpura, petechiae, rashes
- Neurologic: response to exam, hyper or hypotonic, irrepressible movements (sei- zures), primitive reflexes
21
Q
Describe diagnosis: Neonatal Jaundice (14)
A
- To determine if treatment is necessary for unconjugated hyperbilirubinemia, the neonatal serum bilirubin nomogram is used (Figure 18.2).
- Infants are placed in the low-, intermediate-, or high-risk zone depending on their risk factors and gestational age; treatment varies depending on risk zone.
- If greater than 20% of the total bilirubin is conjugated, then further workup should be completed to evaluate for a pathologic cause (see Specialized Tests)
