Acute Liver Failure in Intensive Care

Acute liver failure (ALF) is a rare syndrome characterized by sudden and acute hepatic injury which can be attributed to a number of different causes although not all of them are always clearly identifiable [1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13]. A severe compromise of parenchymal function is followed, at different intervals, by the onset of hepatic encephalopathy, serious haemostasis alteration and, in many cases, multiple organ failure. In the 70s the term FHF (fulminant hepatic failure) had been introduced to describe serious hepatic damage, in absence of known pre-existing hepatic disease, with subsequent onset of encephalopathy within 8 weeks. The syndrome was described as “potentially reversible” [1, 2, 12]. The definition proposed by O’Grady in 1993 and still used today recognizes that the onset of encephalopathy and of altered awareness at different degree is fundamental from a prognostic point of view [2, 12]. Elevated transaminase, hyperbilrubinemia, encephalopathy and serious coagulopathy are the main characteristics of ALF [1, 2, 3, 4, 5, 6, 7, 10]. All the identifying factors that have been proposed include the onset of encephalopathy in the course of ALF, the lack of pre-existing hepatic disease and the high incidence of spontaneous mortality (>85%). This pathology presents itself in a variety of ways and it may be a combination of different aetiologies, each producing a very different outcome. ALF is identifiable by a progressive bilirubin increase [1, 2, 3, 4, 5, 6, 7] within a time span of 7 days to 26 weeks after acute liver damage. Depending on the interval between the onset of jaundice and the clinical signs of encephalopathy, the syndrome is classified as hyper-acute (jaundice-encephalopathy interval: <7 days); acute (jaundice-encephalopathy interval: 8–28 days); sub-acute (jaundice-encephalopathy interval: 28 days–26 weeks). Bernal et al. [1] agree with this classification in the most recent review published on the subject.