The basis of AHF management is supportive therapy in an intensive care setting, aiming to decrease the risk of development of other organ failures and to promote liver regeneration. The role of regenerative agents such as hepatocyte growth factor are still under investigation. Prevention and early treatment of infectious episodes appear to be of great importance.
Plasmapheresis is advocated by groups in Copenhagen and Japan, although controlled trials are needed. Similarly, extracorporeal liver-assist devices are exciting potential developments, although none have yet shown conclusive efficacy in the clinical setting with respect to outcome.
Transplantation remains the treatment of choice for a subgroup of patients with a poor prognosis. A variety of models have been developed, including assessment of liver volume (volumes below 700 cm3 resulting in transplantation), assessment of percentage necrosis on biopsy (complicated by sampling error), and a variety of prognostic models. These need to be simple to apply in the clinical setting and to achieve a high level of sensitivity and specificity in discriminating survivors and non-survivors. Two models are commonly used in Europe. In the first, criteria for poor outcome in non-acetaminophen-induced liver failure have been established as the findings of coma or confusion in association with a factor V level below 20 per cent of normal in patients less than 30 years of age, or below 30 per cent of normal in those aged 30 years or above. In the second, the criteria separate acetaminophen and non-acetaminophen patients. For acetaminophen, the criteria are an arterial pH below 7.3 at greater than 24 h post-overdose and following volume resuscitation, or the concurrent findings of a prothrombin time longer than 100 s (INR > 6.5) plus a creatinine level above 300 pmol/l and grade III/IV encephalopathy. In non-acetaminophen patients the criteria are a prothrombin time longer than 100 s (irrespective of level of encephalopathy) or any three of the following: etiology of seronegative hepatitis or drug-induced liver failure; age less than 10 or more than 40 years; jaundice to encephalopathy time more than 7 days; prothrombin time more than 50 s; serum bilirubin above 300 pmol/l. Comparisons of these two models show them to be equally useful in the clinical setting. They are not applicable to pediatric patients, where different criteria exist, or to specific conditions such as Budd-Chiari syndrome, Wilson's disease, or fatty liver of pregnancy. Transfer to a center offering liver transplantation should ideally be undertaken prior to the development of criteria to allow optimal assessment and time to acquire a suitable graft. Outcome after transplantation is steadily improving; 8-year data from Europe (1988-1996) demonstrate a 52 per cent survival for a group of patients with a predicted 90 per cent mortality by medical management alone. Exciting opportunities are developing with the application of auxiliary liver transplantation which allows for the possibility of immunosuppression withdrawal in patients whose native liver regenerates. This and the progress in the fields of optimizing regeneration and liver support allow great scope for steady improvement in the prognosis of patients with AHF.
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