Phototherapy Plasmapheresis SEVERE HYPERBILIRUBINEMIA IN NEONATES DURING ECMO: IMPORTANT ROLE OF HEMOLYSIS Abhishek Makkar1, 2, Burhan, Mahmood2 , Jon F. Watchko2 1. Division of Neonatology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA 2. Division of Neonatology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA RESULTS I BACKGROUND RESULTS II Postnatal hyperbilirubinemia is frequent in neonates and potentiated by underlying hemolytic conditions. Hemolysis is a known complication of extra corporeal membrane oxygenation (ECMO) . Direct hyperbilirubinemia is also commonly reported in neonates during ECMO. The majority of neonates (27/40 = 68%) demonstrated peak TSB <40% on the Bhutani nomogram. Four infants (10%) developed severe hyperbilirubinemia (peak TSB: 32.8, 23.8, 43.2, 28.5 mg/dl) in conjunction with a rising direct bilirubin (respective peak direct bilirubin:18.2, 8.2, 24.2, 16.2 mg/dl); the direct fraction accounted for 37-68% of TSB. (Table) Three of the 4 infants showed evidence of hemolysis; in one case hemolysis was secondary to use of old blood (10hrs old) to prime the circuit; in another it was associated with a clot in the ECMO circuit (Figure) while in two cases hemolysis occurred during hemofiltration. In addition to phototherapy, plasmapheresis was given in 3 of 4 cases and in all 4 cases circuit change was necessary to control the hyperbilirubinemia. Two of the 4 neonates survived (one death was due to presumed hemochromatosis) and survivors demonstrated normal ABER with no evidence of chronic bilirubin encephalopathy on MRI or exam. One other infant showed elevated direct bilirubin fraction (> 2.0 mg/dL) without severe hyperbilirubinemia. Case # Peak TSB Peak Direct Bilirubin Etiology Intervention Outcome (mg/dl) 1 32.8 18.2 Hemofiltration Circuit Change Died 2 23.8 8.2 Old blood Phototherapy Plasmapheresis Circuit change 3 43.2 24.2 Circuit clot Phototherapy Plasmapheresis Survived 4 28.5 16.2 OBJECTIVES We characterized the incidence and nature of severe hyperbilirubinemia (total serum bilirubin [TSB] ≥20 mg/dl) and clinical risk factors associated with its occurrence in a cohort of neonates managed on ECMO. We determined how hyperbilirubinemia was managed and whether there were any neurologic sequelae specific to their hyperbilirubinemia as indexed by MRI, hearing screens, and neurologic exam at discharge. Table: Peak serum total/direct bilirubin levels and patient outcomes CONCLUSIONS Severe hyperbilirubinemia is uncommon in neonates undergoing ECMO and when it occurs it is accompanied by marked elevations in direct bilirubin. Hemolysis secondary to mechanical factors was observed in most cases of severe hyperbilirubinemia suggesting that the ECMO circuit should be considered as an etiologic mechanism, examined, and changed if necessary to control the hyperbilirubinemia in this population. Addition of hemofiltration components to ECMO circuit may also contribute to significant hemolysis. In addition to phototherapy, Plasmapheresis is an effective early intervention to decrease very high bilirubin levels. METHODS Forty consecutive neonates (≤28 days of life) who underwent ECMO between April 2009 to December 2011 at Children’s Hospital of Pittsburgh, were studied. TSB, direct bilirubin and other clinical labs obtained as part of routine care were analyzed. Details of ECMO support, and clinical course were evaluated. Bilirubin levels were plotted using the Bhutani nomogram. Figure: Large clot seen around the impeller of CentriMag pump