Hepatic encephalopathy | |
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Other names | Portosystemic encephalopathy, hepatic coma,[1] coma hepaticum |
Micrograph of Alzheimer type II astrocytes, as may be seen in hepatic encephalopathy | |
Specialty | Gastroenterology |
Symptoms | Altered level of consciousness, mood changes, personality changes, movement problems[2] slurred speech, Sleep problems, Anxiety or irritability, Muscle twitches (myoclonus), Difficulty concentrating or short attention span, Flapping hand motion (asterixis), Reduced alertness, Cognitive impairment (confused thinking or judgment).[3] |
Complications | hepatic coma.[3] |
Types | Acute, recurrent, persistent[4] |
Causes | Liver failure[2] |
Risk factors | Infections, GI bleeding, constipation, electrolyte problems, certain medications[5] |
Diagnostic method | Based on symptoms after ruling out other possible causes[2][6] |
Differential diagnosis | Wernicke–Korsakoff syndrome, delirium tremens, hypoglycemia, subdural hematoma, hyponatremia[1] |
Treatment | Supportive care, treating triggers, lactulose, liver transplant[1][4] |
Prognosis | Average life expectancy less than a year in those with severe disease[1] |
Frequency | Affects >40% with cirrhosis[7] |
Hepatic encephalopathy (HE) is an altered level of consciousness as a result of liver failure.[2] Its onset may be gradual or sudden.[2] Other symptoms may include movement problems, changes in mood, or changes in personality.[2] In the advanced stages it can result in a coma.[4]
Hepatic encephalopathy can occur in those with acute or chronic liver disease.[4] Episodes can be triggered by infections, gastrointestinal bleeding, constipation, electrolyte problems, or certain medications.[5] The underlying mechanism is believed to involve the buildup of ammonia in the blood, a substance that is normally removed by the liver.[2] The diagnosis is typically based on symptoms after ruling out other potential causes.[2][6] It may be supported by blood ammonia levels, an electroencephalogram, or computer tomography (CT scan) of the brain.[4][6]
Hepatic encephalopathy is possibly reversible with treatment.[1] This typically involves supportive care and addressing the triggers of the event.[4] Lactulose is frequently used to decrease ammonia levels.[1] Certain antibiotics (such as rifaximin) and probiotics are other potential options.[1] A liver transplant may improve outcomes in those with severe disease.[1]
More than 40% of people with cirrhosis develop hepatic encephalopathy.[7] More than half of those with cirrhosis and significant HE live less than a year.[1] In those who are able to get a liver transplant, the risk of death is less than 30% over the subsequent five years.[1] The condition has been described since at least 1860.[1]