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The classic presentation of hepatic encephalopathy is a patient with known cirrhosis who has mental status changes or is in a coma.


  1. A spectrum of reversible neuropsychiatric abnormalities seen in patients with cirrhosis

  2. Must exclude other neurologic or metabolic causes prior to diagnosing hepatic encephalopathy such as:

    1. Diabetic ketoacidosis or hyperglycemic hyperosmolar syndrome

    2. Alcohol intoxication, withdrawal, or Wernicke encephalopathy

    3. Drugs (eg, benzodiazepines, opioids, neuroleptics)

    4. Infection

    5. Electrolyte abnormalities (eg, azotemia, hyponatremia, hypercalcemia)

  3. Overt hepatic encephalopathy (Table 17-5, grades 1–4) is found in 30–45% of patients with cirrhosis.

  4. Minimal hepatic encephalopathy (deficits manifested only on neuropsychological testing) is found in 60% of patients with cirrhosis.

  5. Patients with severe hepatic encephalopathy requiring hospitalization have a 1-year survival rate of < 50%.

  6. Can be precipitated by a wide variety of insults including

    1. Infections

    2. GI bleeding

    3. Constipation

    4. Dehydration

    5. Electrolyte abnormalities

    6. Surgical or intrahepatic shunts (eg, TIPS)

  7. image Always look for the underlying cause of worsening hepatic encephalopathy.

Table 17-5.West Haven Criteria for hepatic encephalopathy.


  1. There is some correlation between the degree of elevation of ammonia (either arterial or venous) and the severity of the encephalopathy, but the ammonia level cannot be used to determine the presence or absence of hepatic encephalopathy.

  2. Diagnosis is based on history and exclusion of other causes of encephalopathy in a patient with significant liver dysfunction.


  1. Identify and treat precipitating causes

  2. Patients with an episode of overt hepatic encephalopathy should be treated indefinitely; the approach to minimal hepatic encephalopathy is evolving.

  3. Treatment focuses on reduction of intestinal accumulation of ammonia.

  4. Lactulose removes both dietary and endogenous sources of ammonia through its cathartic action; it also lowers pH, which reduces the population of urease-producing bacteria, and traps ammonia as ammonium ions in the gut lumen.

    1. First-line treatment for hepatic encephalopathy

    2. Daily dose should be titrated to result in 3 soft stools/day.

    3. Complications include hypovolemia and hypernatremia.

  5. Antibiotics reduce the population of urease-producing bacteria.

    1. Rifaximin in combination with lactulose has been shown to decrease recurrence of hepatic encephalopathy.

    2. Neomycin in combination with lactulose has also been shown to be effective, however its potential to cause ototoxicity and nephrotoxicity limits its use.

  6. Consideration of liver transplantation is indicated in patients with hepatic encephalopathy.

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