The term encephalopathy is very broad and in most cases, is preceded by various terms that describe the reason, cause, or special conditions of the patient that leads to brain malfunction. Hepatic encephalopathy is a worsening of brain function that occurs when the liver is no longer able to remove toxic substances in the blood.
Hepatic encephalopathy is caused by disorders that affect the liver. These include disorders that reduce liver function (such as cirrhosis or hepatitis) and conditions in which blood circulation does not enter the liver.
An important job of the liver is to change toxic substances that are either made by the body or taken into the body (such as medicines) and make them harmless. However, when the liver is damaged, these "poisons" may build up in the bloodstream.
Ammonia, which is produced by the body when proteins are digested, is one of the harmful substances that is normally made harmless by the liver. Many other substances may also build up in the body if the liver is not working well. They can cause damage to the nervous system.
Hepatic encephalopathy may occur suddenly in people who previously had no liver problems when damage occurs to the liver. More often, the condition is seen in people with chronic liver disease.
Hepatic encephalopathy may be triggered by:
- Eating too much protein
- Electrolyte abnormalities (especially a decrease in potassium) from vomiting, or from treatments such as paracentesis or taking
- diuretics ("water pills")
- Bleeding from the intestines, stomach, or esophagus
- Kidney problems
- Low oxygen levels in the body
- Shunt placement or complications (See: Transjugular intrahepatic portosystemic shunt )
- Use of medications that suppress the central nervous system (such as barbiturates or benzodiazepine tranquilizers)
Disorders that can mimic or mask symptoms of hepatic encephalopathy include:
- Alcohol intoxication
- Complicated alcohol withdrawal
- Metabolic abnormalities such as low blood glucose
- Sedative overdose
- Subdural hematoma (bleeding under the skull)
- Wernicke-Korsakoff syndrome
- Hepatic encephalopathy may occur as an acute, potentially reversible disorder. Or it may occur as a chronic, progressive disorder that is associated with chronic liver disease.
HOW IS HEPATIC ENCEPHALOPATHY DIAGNOSED?
A number of specialized tests (psychometric tests) are available for the diagnosis and characterization of HE.
Laboratory tests are also performed for evidence of hepatic biochemical and synthetic dysfunction, and electrolyte disturbances (such as hyponatremia and hypokalemia) that occur as a result of portal hypertension and use of diuretics. In addition, ammonia is the best characterized neurotoxin that precipitates HE.
ACUTE THERAPY: The initial management of overt hepatic encephalopathy type C (ie, caused by cirrhosis and portal hypertension /or systemic shunts) involves two steps:
Identification and correction of precipitating causes
Measures to lower the blood ammonia concentration
CORRECTION OF PRECIPITATING CAUSES: The first step is the identification and correction of precipitating causes.
- Infection (including SBP)
- Gastrointestinal bleeding
- Hypokalemia and/or metabolic alkalosis
- Sedatives or tranquilizers
- Vascular occlusion (hepatic vein or portal vein thrombosis)
Approximately 70 to 80 percent of patients with hepatic encephalopathy improve after correction of precipitating factors
Lower blood ammonia
Lactulose or lactilol