What is hepatic encephalopathy and how does it occur?
When the liver goes into its final stage of disease -also known as liver cirrhosis-, it becomes unable to process various toxins and minerals, most notably ammonia and manganese. Ammonia is produced by bacteria residing in our intestines. When ammonia reaches the blood stream and its level rises, it moves up to the brain. When it passes through the blood-brain barrier, it compromises the function of certain nerve cells called astrocytes.
The damage ammonia and other neurotoxins can exert on the brain is limitless. Early on, some small changes may be noticed including problems with short-term memory and concentration, but later on more severe manifestations may result affecting fine motor skills, sleep cycles, and up to coma. Hepatic encephalopathy can also cause psychiatric changes including depression, paranoia and psychosis. It is estimated that up to 30% of all patients who die of liver failure have severe hepatic encephalopathy, possibly linking it to their mortality.
Some procedures used in the treatment of portal hypertension, which results from liver cirrhosis, can increase the risk of hepatic encephalopathy, especially shunt procedures. Shunting is a method of reducing the pressure on the portal circulation -the circulation between the liver and the small intestines- by directly connecting it to the systemic circulation, bypassing the liver. Although this procedure can be lifesaving in many patients who suffer from severe bloody vomiting, it also helps shunt the mentioned neurotoxins to the brain directly, accelerating hepatic encephalopathy.