Hepatic encephalopathy Hepatic encephalopathy is a neuropsychiatric syndrome caused by liver disease. As it progresses, delirium is followed by coma. Simple delirium needs to be differentiated from delirium tremens and Wernicke's encephalopathy, and coma from subdural haematoma, which can occur in alcoholics after a fall . Features include changes of intellect, personality, emotions and consciousness, with or without neurological signs. The degree of encephalopathy can be graded from 1 to 4, depending on thesep features, and this is useful in assessing response to therapy . When an episode develops acutely, a precipitating factor may be found . The earliest features are very mild and easily overlooked, but as the condition becomes more severe, apathy, inability to concentrate, delirium, disorientation, drowsiness, slurring of speech and eventually coma develop. Convulsions sometimes occur. Examination usually shows a flapping tremor (asterixis), inability to perform simple mental arithmetic tasks or to draw objects such as a star (constructional apraxia; ), and, as the condition progresses, hyper-reflexia and bilateral extensor plantar responses. Hepatic encephalopathy rarely causes focal neurological signs; if these are present, other causes must be sought. Fetor hepaticus, a sweet musty odour to the breath, is usually present but is more a sign of liver failure and poosystemic shunting than of hepatic encephalopathy. Rarely, chronic hepatic encephalopathy (hepatocerebral degeneration) gives rise to variable combinations of cerebellar dysfunction, Parkinsonian syndromes, spastic paraplegia and dementia. Pathophysiology Hepatic encephalopathy is thought to be due to a disturbance of brain function provoked by circulating neurotoxins that are normally metabolised by the liver. Accordingly, most affected patients have evidence of liver failure and poosystemic shunting of blood, but the balance between these varies from individual to individual. Management The principles are to treat or remove precipitating causes and to suppress the production of neurotoxins by bacteria in the bowel. Dietary protein restriction is rarely needed and is no longer recommended as first-line treatment because it is unpalatable and can lead to a worsening nutritional state in already malnourished patients. Lactulose (15-30 mL 3 times daily) is increased gradually until the bowels are moving twice daily. It produces an osmotic laxative effect, reduces the pH of the colonic content, thereby limiting colonic ammonia absorption, and promotes the incorporation of nitrogen into bacteria. Rifaximin (400 mg 3 times daily) is a well-tolerated, non-absorbed antibiotic that acts by reducing the bacterial content of the bowel and has been shown to be effective. It can be used in addition, or as an alternative, to lactulose if diarrhoea becomes troublesome. Chronic or refractory encephalopathy is one of the main indications for liver transplantation. Ref Davidson edition23rd pg865