Wilson disease is a chronic liver disease characterized by cupper overload. This disease is mostly chronic, nevertheless it  may have acute episodes. Fulminant hepatitis due to Wilson Disease is not common.

Fulminant liver failure  of any etiology gives rise to acute encephalopathy. The mechanism of encephalopathy in fulminant liver failure is brain edema, so hyperammonemia is not constant.

In chronic liver diseases complicated with chronic encephalopathy or surgical porto-systemic shunts or TIPPS ammonia is quite relevant.

Thanks Professor Diego for the comment. But I cannot understand what causes encephalopathy due to the brain edema without hyperammonemia. 

Some of it may be due to the cytokine storm from the hepatocyte necrosis. The following article is a good summary of what is the knowledge base on this condition at this point in time-

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3882398/

Dear Go

Causes of brain edema may be multifactorial. Agents like cytokines produced by an injured liver such as IL-6, TNF-alfa and others, reduction of brain arterial blood flux, plasma electrolyte imbalance  and of course hyperammonemia. The precise pathophysiology of brain edema is not clearly known. Nevertheless it is known that hyperammonemia is not present in all cases.

Ammonium has a more recognized role in chronic hepatic encephalopathy. The most efficacious treatments are focused to reduce this agent.