Ammonia: The Old and the New

摘要: Experimental evidence relating increased blood ammonia to cerebral dysfunction dates back 1877 when Eck first created a portocaval shunt. In the 1930’s Van Caulert and Kirk described mental disturbances in cirrhotics receiving ammonium salts.1 However, it wasn’t until 1952 that Gabuzda, Phillips, Schwartz, Davidson2,3 recognized symptoms EEG changes indistinguishable from hepatic encephalopathy could be produced given ammonium-containing cation-exchange resins, salts, urea, or protein orally. Two years later patient with normal liver who had shunt following Whipple procedure for carcinoma of pancreas was reported by McDermoff Adams4 have recurrent episodes irrationality, confusion, disorientation, incontinence, drowsiness, apathy, stupor, sometimes coma Blood abnormalities were correlated manifestations, which reproducible feeding meat, resin, chloride. Such observations patients portacaval shunts been confirmed many times since these early reports, so relationship between clinical syndrome is well established.