An alteration in mental status and cognitive function occurring in the presence of liver failure; may be acute and reversible or chronic and progressive.
Confusion, slurred speech, change in personality that can include being violent and hard to manage, being sleepy and difficult to arouse, asterixis (flapping tremor). Can progress to coma; initially responsive to noxious stimuli, later unresponsive.
Gut-derived neurotoxins that are not removed by the liver because of vascular shunting and decreased hepatic mass reach the brain and cause the symptoms of hepatic encephalopathy. Ammonia levels are typically elevated in encephalopathy, but the correlation between the severity of liver disease and height of ammonia levels is often poor. Other compounds that may contribute include false neurotransmitters and mercaptans.
GI bleeding, azotemia, constipation, high-protein meal, hypokalemic alkalosis, CNS depressant drugs (e.g., benzodiazepines and barbiturates), hypoxia, hypercarbia, sepsis.
TREATMENT: HEPATIC ENCEPHALOPATHY
Remove precipitants; correct electrolyte imbalances. Lactulose (nonabsorbable disaccharide) results in colonic acidification and diarrhea and is the mainstay of treatment; goal is to produce 2–3 soft stools per day. Poorly absorbed antibiotics are often used in pts who do not tolerate lactulose, with alternating administration of neomycin and metronidazole being used to reduce the individual side effects of each. Rifaximin has recently also been used; zinc supplementation is sometimes helpful. Liver transplantation when otherwise indicated.
For a more detailed discussion, see Bacon BR: Cirrhosis and Its Complications, Chap. 365, p. 2058; in HPIM-19.