**3.3.1 Hepatic encephalopathy**

*Hepatic encephalopathy* in decompensated cirrhosis shares several qualities with the encephalopathy observed in ALF, including the grades of severity. However, major differences exist in clinical presentation and management of hepatic encephalopathy in ACLF. The chronicity of portal hypertension allows time for the development of ammonia fixation mechanisms and neuronal adaptation to ammonia. Thus, the hepatic encephalopathy of ACLF is not typically associated with cerebral edema. Treatment is supportive and focuses on patient safety and avoidance of complications. As in ALF, patients with grade III or IV encephalopathy warrant elective intubation for airway protection. Causative factors of hepatic encephalopathy include dehydration, overdiuresis, infection, use of benzodiazepines and narcotics, gastrointestinal bleeding, constipation, electrolyte or acid-base imbalances, or recent transjugular intrahepatic portosystemic shunt (TIPS) procedure. Progression of underlying liver disease may be the only identifiable precipitant; when reversible causes are identified, they should be treated.

Medical treatment of hepatic encephalopathy consists of oral agents to assist in toxin elimination. Lactulose and other nonabsorbable disaccharides improve intestinal excretion of nitrogen and reduce production of ammonia by enteric bacteria. Intestinal decontamination with oral antibiotics such as rifaximin or metronidazole reduces the burden of ammoniaproducing bacteria.
