Hepatic encephalopathy
Also known as hepatic coma, hepatic encephalopathy is a neurologic syndrome that results from the liver’s failure to detoxify noxious agents that arise from the GI tract. Most common in patients with cirrhosis, this syndrome is caused primarily by ammonia intoxication of the brain. It may be acute and self-limiting or chronic and progressive.
Treatment requires correction of the precipitating cause and reduction of blood ammonia levels. In advanced stages, the prognosis is extremely poor, despite vigorous treatment.
Causes
Hepatic encephalopathy develops as a result of rising blood ammonia levels. Several factors cause these levels to rise.
Improper shunting of blood
Normally, the ammonia produced by protein breakdown in the bowel is metabolized to urea in the liver. When portal blood shunts past the liver, ammonia directly enters the systemic circulation and is carried to the brain.
Such shunting may result from the collateral venous circulation that develops in portal hypertension or from surgically created portal-systemic shunts. Cirrhosis further compounds this problem because impaired hepatocellular function prevents conversion of ammonia that reaches the liver.
Other factors
Other factors that predispose to rising ammonia levels include excessive protein intake, sepsis, excessive accumulation of nitrogenous body wastes (from constipation or GI hemorrhage), and bacterial action on protein and urea to form ammonia.
Certain other factors heighten the brain’s sensitivity to ammonia intoxication, including fluid and electrolyte imbalances (especially metabolic alkalosis), hypoxia, azotemia, impaired glucose metabolism, infection, and administration of sedatives, narcotics, and general anesthetics.
