The occurrence of hyperbilirubinaemia after heart surgery using cardiopulmonary bypass or post-operative heart failure is fairly common. Mechanism of hyperbilirubinemiais still not completely clarified, and there are so few specific therapies available for acute hepatobiliary injury. Post-operative mortality well correlates with increasing total bilirubin values, particularly for bilirubin-associate acute kidney tubular necrosis. The difficulty to reduce mortality is partially a consequence of not completely understood physiopathology. It is obvious that long-lasting CPB plays an important role, in association with hemodilution, hypotension, ischemia-reperfusion, and increasing hematic level of endogenous catecholamine with reduction of hepatic blood flow. Case report. A 68 years old man with severe mitral valve regurgitation and pulmonary hypertension and low EF 30%. Mitral valve replacement and tricuspid anuloplastic was performed. Due to low cardiac output syndrome severe hyperbilirubiemeia was seen (24 mg/dl. and unconjugated fraction 16mg/dl) days after. Phenobarbital (luminal) was started 15 mg/kg daily. Two days later the level decreased until 8 mg/dl with normalization of conjugation/unconjugation ratio.Postoperative hyperbilirubinemia is a multifactorial process caused by both impaired liver function of bilirubin transport. In case of elevated level of unconjugated fraction we suggest to use Luminal as alternative for decreasing unconjugated fraction.
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