Hepatic Encephalopathy

  1. General information
    1. Frequent terminal complication in liver disease
    2. Diseased liver is unable to convert ammonia to urea, so that large quantities remain in the systemic circulation and cross the blood/brain barrier, producing neurologic toxic symptoms.
    3. Caused by cirrhosis, GI hemorrhage, hyperbilirubinemia, transfusions (particularly with stored blood), thiazide diuretics, uremia, dehydration
  2. Assessment findings
    1. Early in course of disease: changes in mental functioning (irritability); insomnia, slowed affect; slow slurred speech; impaired judgment; slight tremor; Babinski's reflex, hyperactive reflexes
    2. Progressive disease: asterixis, disorientation, apraxia, tremors, fetor hepaticus, facial grimacing
    3. Late in disease: coma, absent reflexes
    4. Diagnostic tests
      1. Serum ammonia levels increased (particularly later)
      2. PT prolonged
      3. Hgb and hct decreased
  3. Nursing interventions
    1. Conduct ongoing neurologic assessment and report deteriorations.
    2. Restrict protein in diet; provide high carbohydrate intake and vitamin K supplements.
    3. Administer enemas, cathartics, intestinal antibiotics, and lactulose as ordered to reduce ammonia levels.
    4. Protect client from injury: keep side rails up; provide eye care with use of artificial tears/eye patch.
    5. Avoid administration of drugs detoxified in liver (phenothiazines, gold compounds, methyldopa, acetaminophen).
    6. Maintain client on bed rest to decrease metabolic demands on liver.

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