Hepatic Encephalopathy
Basic Information 
Clinical Presentation
History, Chief Complaint
Physical Exam Findings
• Other signs of hepatic disease may be present, including icterus, hepatic photosensitization, weight loss, and coagulopathy.
• A complete neurologic examination should be performed. Cranial nerve function is typically intact, although bilateral laryngeal paralysis may occur. In addition to the behavioral changes listed above, ataxia and central blindness (lack of a menace response with normal pupillary light reflexes) may be present.
Etiology and Pathophysiology
• Acute astrocyte swelling, cytotoxic cerebral edema, and intracranial hypertension
• Gastrointestinal (GI)-derived neurotoxins that are incompletely cleared by the failing liver (eg, increased blood ammonia, mercaptans, short chain fatty acids, and phenol concentrations)
• Augmented activity of cerebral inhibitory neurotransmitter systems such as γ-aminobutyric acid, serotonin, and benzodiazepine (eg, glutamate) with concurrent depression of excitatory pathways
• Increased inflammatory cytokine expression and neurosteroid synthesis
• False neuroinhibitory transmitter accumulation (eg, phenylethanolamine, serotonin, octopamine) in the brain as a consequence to an increased ratio of aromatic amino acid (phenylalanine, tyrosine, tryptophan) to branch chain (valine, leucine, isoleucine) amino acids in the blood
• Impaired central nervous system metabolism secondary to energy depletion
