Hepatic encephalopathy (HE) is a significant complication of both acute and chronic liver disease, causing much morbidity and mortality. It is a complex neuropsychological condition, associated with hyperammonaemia and systemic inflammation, with a wide spectrum of symptoms. The West Haven criteria describe grades of severity from 0 (subclinical) and I (changes in awareness, mood, attention, cognition, and sleep pattern) through to IV (coma). It is further classified by the underlying aetiology: type A, due to acute liver failure; type B, secondary to portosystemic shunting; and type C, occurring in chronic liver disease in association with precipitating factors including infections, gastrointestinal bleeding, and electrolyte disorders, particularly hyponatraemia. There is no definitive test or set of diagnostic criteria to establish a diagnosis of HE, which remains primarily a clinical diagnosis of exclusion in patients with a history or clinical evidence of liver disease. Management depends on the type of HE, but for type C (the commonest type) typically includes lactulose and rifaximin. Patients with cirrhosis with ongoing overt HE despite optimal medical management have a dismal outlook and should be considered promptly for liver transplantation.
Clinical management of type C hepatic encephalopathy