This article considers the pathogenesis of hepatic coma. Molecular mechanisms involving possible disorders in cerebral transmitters are related to the most salient fact about hepatic coma: the liver-brain axis. Various competing, but not necessarily mutually exclusive, theories are examined for relevance and compatibility with clinical and experimental information. Evidence is presented against the role of ammonia as the sole factor in the pathogenesis of coma. Known amino acid imbalances in hepatic coma are related to possible disturbances in neurotransmitters in the brain and the role of false neurotransmitters examined. Therapy is related to biochemical mechanisms.
Fischer JE. Hepatic Coma in Cirrhosis, Portal Hypertension, and Following Portacaval ShuntIts Etiologies and the Current Status of Its Treatment. Arch Surg. 1974;108(3):325-336. doi:10.1001/archsurg.1974.01350270055010