Clinical manifestations

A. Hepatic encephalopathy manifests as mild changes in personality to altered motor functions and/or level of consciousness.

B. Most episodes are precipitated by identifiable factors, including gastrointestinal bleeding, excessive protein intake, constipation, excessive diuresis, hypokalemia, hyponatremia or hypernatremia, azotemia, infection, poor compliance with lactulose therapy, sedatives (benzo-diazepines, barbiturates, antiemetics), hepatic insult (alcohol, drugs, viral hepatitis), surgery, or hepatocellular carcinoma.

C. Hepatic encephalopathy is a diagnosis of exclusion. Therefore, if a patient with acute or chronic liver failure suddenly develops altered mental status, concomitant problems must be excluded, such as intracranial lesions (hemorrhage, infarct, tumor, abscess), infections (meningitis, encephalitis, sepsis), metabolic encephalopathies (hyperglycemia or hypoglycemia, uremia, electrolyte imbalance), alcohol intoxication or withdrawal, Wernicke's encephalopathy, drug toxicity (sedatives, psycho-active medications), or postictal encephalopathy.

D. Physical exam may reveal hepatosplenomegaly, ascites, jaundice, spider angiomas, gynecomastia, testicular atrophy, and asterixis.

E. Computed tomography may be useful to exclude intracranial abscess or hemorrhage. Laboratory evaluation may include serum ammonia, CBC, electrolyte panel, liver profile, INR/PTT, UA, and blood cultures.

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