- Albumin determines the exchangeable bilirubin pool via high affinity binding; administer bilirubin-free albumin to manage hazardous hyperbilirubinaemia and reduce neurotoxicity risk.
- Albumin priming before double volume exchange transfusion increases albumin mass and binding capacity, enhancing bilirubin clearance and immediate neuroprotection during the pre-exchange period.
- Prime early in neonates with intermediate to advanced acute bilirubin encephalopathy for neuroprotection; consider preventive priming when bilirubin to albumin ratios near saturation.
Semin Perinatol. 2026 Aug 24:152292. doi: 10.1016/j.semperi.2026.152292. Online ahead of print.
ABSTRACT
Albumin is the crux of the exchangeable (i.e., miscible) bilirubin pool, controlling via its high affinity binding the distribution of bilirubin within and across the intravascular and extravascular spaces. It follows that clinicians should leverage the administration of bilirubin free albumin in the management of hazardous hyperbilirubinemia to avoid or reverse bilirubin neurotoxicity. A standard double volume exchange transfusion does exactly that via the albumin laden fresh frozen plasma used to reconstitute the blood infused during the procedure. Albumin priming – the infusion of bilirubin-free albumin prior to a double volume exchange transfusion – augments the infant’s pre-exchange albumin mass and albumin bilirubin binding capacity. As such, albumin priming can enhance bilirubin clearance over the course of the subsequent exchange transfusion and provide an immediate stepwise gain in neuroprotection during the pre-exchange period. The potential for neuroprotection against worsening bilirubin-induced neurological dysfunction is the principal reason to albumin prime and prime early when caring for a neonate with signs of intermediate to advanced stage acute bilirubin encephalopathy. Albumin priming should also be considered in asymptomatic infants whose bilirubin – albumin molar ratios approach or exceed albumin’s saturable binding limits, as a preventive measure to attenuate bilirubin neurotoxicity risk.
PMID:42637606 | DOI:10.1016/j.semperi.2026.152292
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