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Hepatic encephalopathy (sometimes hepatoencephalopathy) is a potentially-reversible neuropsychiatric abnormality in the setting of liver failure, whether chronic (as in cirrhosis), or acutely. It can be diagnosed only after exclusion of other neurological, psychiatric, infectious, and metabolic etiologies.
With severe liver impairment, toxic substances normally removed by the liver accumulate in the blood and impair the function of brain cells. If there is also portal hypertension, and subsequent bypassing of the liver filtration system of blood flowing in from the intestines, these toxic substances can travel directly to the brain, without being modified or purified. Signs can include impaired cognition, a flapping tremor (asterixis), and a decreased level of consciousness including coma (hepatic coma or coma hepaticum), cerebral edema, and, ultimately, death.
Hepatic encephalopathy leads to changed cognitive function. This can range from subtle deficits in higher mental functions (in mild cases) to obtundation and coma (in severe cases). Left untreated, severe hepatic encephalopathy can cause death.
One of the earliest manifestations of hepatic encephalopathy is “day-night reversal.” In other words, affected individuals tend to sleep during the day and stay awake at night. Another early manifestation is impairment in spatial perception. This can be made apparent by noting the patient’s poor ability to copy or draw various simple images, e.g., cube, star, clock. This deficit can also be demonstrated by administering a test that has the patient connect a number of randomly-placed dots on a sheet of paper (the “trail test” or “numbers connecting test”).
In addition to changed level of consciousness, the hallmark of hepatic encephalopathy on the physical examination is the presence of asterixis. This is detected by having the patient hold out their outstretched arms and hands while cocking their wrists back. In the presence of asterixis, there is a non-synchronized, intermittent flapping motion at the wrists. Asterixis is not specific to hepatic encephalopathy. It may also be seen in states such as renal failure and carbon dioxide retention.
The inhibitory control test (ICT) may be a faster way to diagnose hepatic encephalopathy than standard psychometric tests (average administration time of 15 minutes versus 37 minutes) [1]
Although the onset of hepatic encephalopathy may simply reflect worsening of underlying liver disease, it may also be due to a number of independent factors, each treatable in its own right. In fact, studies have shown that the majority of cases are due to one (or more) of such precipitating factors. It is critical, then, that a search for possible precipitants be conducted in patients with new-onset hepatic encephalopathy, and specific treatment initiated if such a precipitant is discovered.
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