Abstract
The mortality of acute liver failure remains unacceptably high and liver transplantation is the only effective treatment available to date. This review focuses on new research developments in the field and aims to provide a pragmatic organ-based treatment approach for liver failure patients requiring intensive care support. The pathophysiological basis for cerebral edema formation in acute liver failure continued to be the focus of various investigations. In-vivo observations confirmed the link between ammonia, cerebral glutamine content and intracranial hypertension. The role of arterial ammonia as an important prognostic indicator formed the basis of prospective, observational studies. Reduced monocytic HLA-DR expression linked acute liver failure with poor prognosis, and the cerebral effects and side effects of vasoactive therapy with terlipressin were investigated with two studies showing contradictory results. Despite increased knowledge of the pathophysiological events leading to organ dysfunction in acute liver failure, supportive treatment options remain limited in their efficacy and largely noncurative.
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