One of the most easily preventable causes of brain injury from severe neonatal jaundice. Neonatal hyperbilirubinaemia with signs of acute encephalopathy is a neurological emergency
- Neonatal Jaundice with bilirubin > 360 micromoles/L
- 50-60 % of all term newborns are jaundiced in the first week of life.
- Total serum bilirubin peaks at age 3-5 d (later in Asian infants).
- Free Bilirubin crosses the blood-brain barrier when the
blood binding capacity is exceeded
- Causes Bilirubin-induced neurologic dysfunction
- Most of the circulatory bilirubin is bound to
albumin which acts as a "neuroprotective"
- Bilirubin damages brain tissue cells via necrosis and apoptosis,
- Sleepy, less responsive
- hypotonia /hypertonia /opisthotonus
- Sensorineural hearing loss due to damage to the cochlear nuclei.
- Severe encephalopathy
Factors predisposing to neurotoxicity of unconjugated hyperbilirubinemia
- Bilirubin concentration exceeds the binding capacity of serum albumin
- Displacement of bilirubin from albumin by acidosis or certain drugs (e.g.,
- Sepsis, Preterm infants due to risk due to lower serum albumin concentrations and risk for acidosis and sepsis.
- FBC, U&E, LFTS, Coomb's test, sepsis screen
- Bilirubin levels < 323 less harmful. Bilirubin > 360 micromoles/L needs treatment. Follow local treatment thresholds
- MR appearance of kernicterus (bilirubin encephalopathy). T2-weighted images show a high signal bilaterally in the globus pallidus, a known area of cerebral deposition of bilirubin.
- Emergency: Neonatal hyperbilirubinaemia with signs of acute encephalopathy is a neurological emergency for Intense UV phototherapy whilst prepare for exchange transfusion
- Phototherapy and balanced exchange transfusions. Treatment levels depend upon the maturity