Hepatic Encephalopathy

Pathophysiology of Hepatic Encephalopathy

Hepatic encephalopathy is a:

1) neuropsychiatric disturbance caused by cirrhosis/hepatocellular dysfunction and shunting of portal venous blood into the systemic system with bypass of the liver
2) exact mechanism is unknown – likely ammonia level is involved
3) typically follows a precipitating event (like GI bleeding or infection) in a stable cirrhotic

Signs and Symptoms

1) personality changes
2) decreased mental status (confusion to frank coma due to cerebral edema)
3) asterixis
4) rigidity
5) hyperreflexia
6) extensor plantar signs

Associated Conditions

increased incidence of hepatic encephalopathy in –

1) GI bleeding
2) infection
3) increased dietary proteins
4) hypokalemic alkalosis (excessive vomiting or diarrhea)
5) benzodiazepine use
6) physiologic stress (surgery)

Biochemistry

in hepatic encephalopathy the following are increased –

1) ammonia
2) permeability of blood-brain barrier
3) endogenous benzodiazepines
4) GABA
5) mercaptans (methionine byproducts)
6) phenol
7) short chain fatty acids
8) octopamine (a false neurochemical transmitter secondary to abnormal amounts of branched-chain and aromatic amino acides)

Treatment

1) elimination of precipitating factor
2) evacuation of blood from lower GI tract (via enemas/laxatives)
3) low-protein diet
4) lactulose
5) oral nonabsorbably antibiotics (neomycin)
6) metronidazole
7) refaximin
8) barbituate coma in severe cases

Tips for USMLE

1) not all hepatic encephalopathy patients have increased ammonia levels (and levels do not correspond to severity)
2) asterixix occurs in other conditions (renal failure, hypercapnia, lead poisoning, drug overdose (especially the anticonvulsants)