Neonatal Jaundice
conjugated = direct
unconjugated = indirect
<48h
Febrile/unwell > work up for sepsis AND Ix jaundice
Bilirubin (total/conjugated)
FBE (Haemolysis/polycyth), Film (red cell defects) Retics
Group and DAT (Coombs reagent is an antibody-antibody whic looks for mums antibodies on babys red cells)
<2w and all investigations NAD > physiologic, resolved in 2w (3 for prem)
>2w and all investigations NAD > breast milk jaundice (a factor in human milk deconjugates the bilirubin > reabsorbed)
Gilberts syndrome: impaired glucuronidation (conjugation) to 30% of normal. benign can be exacerbated by exercise/stress/haemolysis
Crigler najjar I: same gene but defect is in actual gene (rather than in promoter sequence before gene) leading to abnormal protein rather than reduced amounts of normal protein. Fatal without PT or plasmaphoresis (bilirubin is bound to albumin)
CN II: same as CNI but isolated point mutation substituting a single amino acid leading to modest reduction in activity of the enzyme.
Plethora
cephalohaematoma/bruising
Hepatomegaly (hepatitis/metabolic)
GIT obstruction > surgeons
Rx
sunlight not recommended
hydration (monitor hydration/wt)
PT (monitor bili/EUC) recheck 6 hours after starting
FU
if <3d / still establishing feeds / borderline or rising
RV if pale stools, dark urine, lethargic, poor feeding, unwell, or persists beyond
Complications
Kernicterus
unconjugated = indirect
<48h
- haemolysis
- isoimmune ABO, Rhesus, other
- Red cell defects: spherocytosis
- G6PD (lack of enzyme that protect reed cells from oxid injury)
Febrile/unwell > work up for sepsis AND Ix jaundice
Bilirubin (total/conjugated)
FBE (Haemolysis/polycyth), Film (red cell defects) Retics
Group and DAT (Coombs reagent is an antibody-antibody whic looks for mums antibodies on babys red cells)
- Conjugated (10%) (pale stools, dark urine) DW Gastroenterology
- LFT, TFT, Septic screen, viral serology, A1AT, Abdo US, see conjugated
- haemolysis > DW Haematology
- Above treatment > PT DW Neonatologist
- Urine MCS/reducing sub, EUC, TFT, G6PD
- >2w below treatment without clear cause (haemolysis/cephalo/plethora) DW Paed
- Urine MCS, reducing substance, G6PD
<2w and all investigations NAD > physiologic, resolved in 2w (3 for prem)
>2w and all investigations NAD > breast milk jaundice (a factor in human milk deconjugates the bilirubin > reabsorbed)
Gilberts syndrome: impaired glucuronidation (conjugation) to 30% of normal. benign can be exacerbated by exercise/stress/haemolysis
Crigler najjar I: same gene but defect is in actual gene (rather than in promoter sequence before gene) leading to abnormal protein rather than reduced amounts of normal protein. Fatal without PT or plasmaphoresis (bilirubin is bound to albumin)
CN II: same as CNI but isolated point mutation substituting a single amino acid leading to modest reduction in activity of the enzyme.
Plethora
cephalohaematoma/bruising
Hepatomegaly (hepatitis/metabolic)
GIT obstruction > surgeons
Rx
sunlight not recommended
hydration (monitor hydration/wt)
PT (monitor bili/EUC) recheck 6 hours after starting
- photoisomerisation to more soluble form
FU
if <3d / still establishing feeds / borderline or rising
RV if pale stools, dark urine, lethargic, poor feeding, unwell, or persists beyond
Complications
Kernicterus