Hepatic encephalopathy risk factors
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Risk Factors
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.
Virtually any metabolic disturbance may precipitate hepatic encephalopathy. Common culprits are hyponatremia (often arising as a result of diuretic treatment or simply as a complication of the edema typically found in advanced cirrhosis), hypokalemia (again, often as a result of diuretic use), alkalosis, dehydration, hypoglycemia (a condition to which people with cirrhosis are susceptible), and renal failure of even mild degree.
Likewise, there are a number of medications the use of which may bring on hepatic encephalopathy. These include benzodiazepines (e.g. diazepam, lorazepam), narcotics, and diuretics. Alcohol ingestion, whether or not it was the cause of the patient's liver disease, may also precipitate hepatic encephalopathy.
Infection is an important precipitant of hepatic encephalopathy. In some cases, the only clinical manifestation of the infection is the development of the encephalopathy. In fact, this is a frequent phenomenon in patients whose ascites has become infected (i.e. spontaneous bacterial peritonitis).
Sometimes, hepatic encephalopathy arises as a result of patient non compliance with dietary protein restriction. Indeed, given the general lack of palatability of low protein diets, non-compliance is common and, hence, so is its effect to precipitate encephalopathy.
Bleeding into the stomach or small intestine (both of which occur with increased frequency in people with liver disease and/or portal hypertension) may also lead to hepatic encephalopathy. Blood contains large quantities of protein in the form of plasma proteins and hemoglobin. Hence, the presence of blood in the stomach or small intestine represents a protein load which, as a result of bacterial metabolism in the lumen of the gut, is converted to potentially toxic products such as ammonia.
Certain surgical procedures employed to treat portal hypertension commonly lead to the development of hepatic encephalopathy. For example, operations to relieve pressure in the portal vein by connecting it to the splenic vein or other systemic venous vessels, have the effect of diverting incoming intestinal venous blood away from the liver. This means that such ammonia-carrying blood will not be able to be "purified" by the liver. Encephalopathy can result. Similarly, the more recently developed "TIPS" procedure (transjugular intrahepatic portosystemic shunt) often precipitates hepatic encephalopathy (~30 percent of patients undergoing it).