Paeds Vivas · fetal-neonatal-and-perinatal
Neonatal jaundice: unconjugated hyperbilirubinaemia: Viva
Branching clinical structured oral on neonatal unconjugated hyperbilirubinaemia: risk assessment, hour-specific nomogram interpretation, phototherapy and exchange transfusion decisions, and kernicterus prevention.
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Target exams
Branch 1: Risk assessment and interpretation
The candidate should immediately recognise that jaundice within the first 24 hours of life is always pathological and requires urgent evaluation. A TSB of 220 micromol per litre at 20 hours in a term infant is significantly elevated for age and falls in the high-risk zone on the hour-specific nomogram. The maternal blood group O raises the possibility of ABO incompatibility if the infant is group A or B. [3]
The candidate should list the risk factors: onset before 24 hours, maternal blood group O (potential ABO incompatibility), and any additional risk factors to be elicited from the history including gestational age, feeding adequacy, weight loss, cephalohaematoma or bruising, family history of jaundice or G6PD deficiency, and ethnic background. The investigation should include a haemolytic workup: DAT, blood group, full blood count with reticulocyte count, peripheral film, and G6PD assay if at-risk heritage. [3]
The 2022 AAP guideline uses gestational-age-specific threshold curves with a neurotoxicity risk modifier. For a 39-week well infant with no haemolysis, this bilirubin may or may not meet the phototherapy threshold depending on the exact age in hours. If the DAT is positive (haemolysis confirmed), the infant is classified as higher neurotoxicity risk, which lowers the threshold. [1]
Branch 2: Investigation and management
The haemolytic workup confirms ABO incompatibility: the infant is blood group A, DAT is positive, and the peripheral film shows spherocytes with an elevated reticulocyte count. The candidate should now interpret this as immune-mediated haemolysis requiring intensive phototherapy at a lower threshold. [3]
Phototherapy should be initiated with high-intensity blue LED light at 430 to 490 nm, irradiance above 30 microwatts per square centimetre per nanometre, and maximal skin surface exposure. The eyes are protected, temperature is monitored, and feeding is continued. The TSB should be repeated at 4 to 6 hours. If the bilirubin continues to rise despite intensive phototherapy in confirmed immune haemolysis, intravenous immunoglobulin at 0.5 to 1 g per kg over 2 hours is indicated to reduce haemolysis and potentially avoid exchange transfusion. [3]
The candidate should define the exchange transfusion threshold using the 2022 AAP gestational-age-specific curves for a higher-risk infant and prepare blood cross-matched against both mother and infant if the threshold is approached. [1]
Branch 3: Kernicterus prevention and counselling
The candidate should demonstrate knowledge of acute bilirubin encephalopathy signs: early (lethargy, hypotonia, poor suck, high-pitched cry), intermediate (hypertonia, retrocollis, opisthotonos, fever), and advanced (apnoea, seizures, coma). Any neurological signs mandate immediate exchange transfusion regardless of the exact TSB value. [2]
The chronic sequelae of kernicterus include athetoid cerebral palsy, sensorineural hearing loss, upward gaze palsy, and cognitive impairment. The bilirubin-induced neuronal injury involves mitochondrial dysfunction, oxidative stress, excitotoxicity, and apoptosis, preferentially affecting the basal ganglia, cochlear nuclei, and brainstem. [2]
When counselling parents, the candidate should explain that the jaundice is caused by a mismatch between the mother's and baby's blood groups causing mild red cell breakdown, that phototherapy is a safe and effective treatment using special blue light, that breastfeeding should continue, and that the baby will be monitored closely until the bilirubin has fallen to safe levels. The parents should be reassured that kernicterus is preventable with appropriate treatment and that the outlook is excellent when caught early. [1]
References
- [1]Kemper AR Clinical Practice Guideline Revision: Management of Hyperbilirubinemia in the Newborn Infant 35 or More Weeks of Gestation. Pediatrics, 2022.PMID 35927462
- [2]Watchko JF Bilirubin-induced neurologic damage--mechanisms and management approaches. N Engl J Med, 2013.PMID 24256380
- [3]American Academy of Pediatrics Subcommittee on Hyperbilirubinemia Management of hyperbilirubinemia in the newborn infant 35 or more weeks of gestation. Pediatrics, 2004.PMID 15231951