Purpose of review: Brain disturbances, which are considered a form of hepatic encephalopathy, are common in acute-on-chronic liver failure.
Recent findings: Patients with hepatic encephalopathy exhibit sings of energy impairment that may participate in the development of disturbances in neurotransmission. Ammonia participates in the genesis of brain edema and in the development of oxidative stress injury to astrocytes. Neuroinflammation is a new element that has been described in experimental models. These mechanisms are involved in the genesis of cognitive sequels that may persist after liver transplantation. Clinical trials have demonstrated the value of drugs that decrease the production of ammonia in the intestines to prevent encephalopathy. In addition, improvement of circulatory dysfunction with the use of albumin and vasoconstrictors may prevent hepatic encephalopathy in acute-on-chronic liver failure. New drugs that act by enhancing ammonia disposal through the synthesis of nitrogenous metabolites have shown promising results.
Summary: A better knowledge of the pathogenesis of brain disturbances in acute-on-chronic liver failure provides the rationale for using ammonia-focused therapy in the prevention and treatment of encephalopathy. New therapies addressed to correct brain edema, circulatory dysfunction and inflammation may also be useful for encephalopathy and may improve the neurological outcome.