Hyperbilirubinemia occurs in up to 40% of critically ill. In ICU, hyperbilirubinemia is an independent factor that influences patients' morbidity and mortality. Jaundice can reflect the course of disease or be caused by treatment (e.g. extracorporeal membrane oxygenation (ECMO)), thus can be difficult to differentiate. Sepsis was also associated with development of jaundice secondary to intrahepatic cholestasis. Prolonged cholestasis should be addressed to avoid liver damage. The patient with diagnosis of septic shock and severe acute respiratory distress syndrome was retrieved to our hospital for ECMO. Three days after initiation of ECMO, the patient developed jaundice, with increase of bilirubin, Gamma-glutamyltransferase and Alkaline phosphatase, without elevation of alanine aminotransferase and INR. Although ECMO was stopped, bilirubin serum levels were increasing, reaching the peak of 18.41 mg/dL of total and 15.67 mg/dL of direct bilirubin. Abdominal computed tomography showed homogeneous liver and non-dilated bile ducts. Viral hepatitis was excluded. CIOMS/RUCAM score was 0. Sepsis-related cholestasis was diagnosed. Despite cessation of sedation, the patient remained unconscious. Hemoadsorption therapy was initiated due to prolonged high levels of conjugated bilirubin. After 48 h of CytoSorb treatment, total bilirubin level was decreased to 2.4 mg/dL, the patient regained spontaneous eyes opening and could be transferred to regional hospital. Hyperbilirubinemia did not return in 3 months. Sepsis-related cholestasis is a diagnosis of exclusion that should be considered in case of jaundice in critically ill patients. In our patient, CytoSorb was a useful therapeutic option in prolonged cholestasis. Adsorption therapy was able to facilitate long-term regain of balance between inflammatory process, cytokine production and bilirubin turnover in the liver.
Keywords: ECMO; Sepsis; acute respiratory distress syndrome; apheresis and detoxification techniques; artificial kidney; intrahepatic cholestasis.