1. etiologies of unconjugated hyperbilirubinemia
1.1. decreased hepatic clearance
1.1.1. Crigler-Najar 1 and 2
1.1.1.1. really broken UGT1A1
1.1.2. Gilbert syndrome
1.1.2.1. Kind of broken UGT1A1
2. screening for hyperbilirubinemia
2.1. clinical assessment
2.2. Risk Factors
2.2.1. ABO/Rh incompatibility
2.2.2. prematurity
2.2.3. bruising/trauma, cephalohematoma
2.2.4. East Asian race
2.2.5. exclusive breastfeeding
2.2.6. siblings w/ jaundice
2.3. serum total & direct bili levels
2.4. may use Bhutani nomogram or Bili calculator to treat
2.5. careful discharge planning/f/u
3. Management of unconjugated bilirubin
3.1. Hydration/Feeding
3.2. Phototherapy
3.3. Exchange transfusion
3.4. sunny window is not evidence-based!
4. bilirubin catabolism
4.1. RBC lysis-waste products-->unconjugated bilirubin
4.1.1. bilirubin binds to albumin-->liver--> conjugated from lipid-soluble to water-soluble from UGT1A1 enzyme
4.1.1.1. conjugated bilirubin--> bile ducts--> intestines--> excreted in stool
4.1.1.1.1. some conjugated bilirubin can become unconjugated thru Beta-glucuronidase(enterohepatic recirculation)
5. Benign Neonatal Hyperbilirubinemia/physiologic jaundice
5.1. peaks @ 48-96hrs of life (7-9mg/dl)
5.1.1. resolves by 2 weeks; increased breakdown of fetal RBCs; immature/inefficient liver; increased enterohepatic circulation
5.2. Increased production due to hemolysis of RBCs
5.2.1. ABO or Rh incompatibility
5.2.1.1. RBC membrane defects
5.2.1.1.1. erythrocyte enzyme defects; birth trauma; sepsis
6. Treatment/Outcomes
6.1. Bilirubin-induced neurologic dysfunction (BIND)
6.1.1. Cytologic & molecular damage to basal ganglia from unconjugated bilirubin
6.2. Acute bilirubin encephalopathy(ABE)
6.2.1. seizures
6.2.2. encephalopathy
6.2.3. lethargy
6.3. Chronic bilirubin encephalopathy(CBE)
6.3.1. AKA Kernicterus
6.3.2. Chronic & permanent sequelae
6.3.3. sensorineural hearing loss
6.3.4. Cerebral palsy