Acute liver failure caused by fulminant hepatitis has at least 2 components—severe impairment or absence of liver function, and the effects of tissue destruction. The former effect can be simulated by rendering animals anhepatic. With adequate restoration of vascular connections, such animals will awake from anesthesia and appear normal for up to 60 hours. Even terminally, such animals seldom show features of hepatic encephalopathy, but rather of respiratory failure. This model is reasonably easy to reproduce; not so the attempts to use toxins or ischemia to simulate a human disease that probably occurs with recurrent waves of destruction compounding damage.
Hickman R. An Improved Model of Acute Liver Failure Based on Transient Ischemia of the Liver—Invited Critique. Arch Surg. 2000;135(10):1189. doi:10.1001/archsurg.135.10.1189