Hepatic encephalopathy, or portosystemic encephalopathy (PSE), is a life-threatening complication of liver disease that occurs with profound liver failure. Ammonia is considered the major etiologic factor in the development of encephalopathy. Patients have no overt signs but do have abnormalities on neuropsychologic testing. Hepatic encephalopathy is the neuropsychiatric manifestation of hepatic failure associated with portal hypertension and the shunting of blood from the portal venous system into the systemic circulation. Circumstances that increase serum ammonia levels precipitate or aggravate hepatic encephalopathy, such as digestion of dietary and blood proteins and ingestion of ammonium salts. Other factors that may cause hepatic encephalopathy include excessive diuresis, dehydration, infections, fever, surgery, some medications and, additionally, elevated levels of serum manganese and changes in the types of circulating amino acids, mercaptans, and levels of dopamine and gamma-aminobutyric acid (GABA) neurotransmitters in the central nervous system.

• Earliest symptoms of hepatic encephalopathy include minor mental changes and motor disturbances. Slight confusion and alterations in mood occur; the patient becomes unkempt, experiences disturbed sleep patterns, and tends to sleep during the day and to experience restlessness and insomnia at night.
• With progression, patient may be difficult to awaken and be completely disoriented with respect to time and place; with further progression, the patient lapses into frank coma and may have seizures.
• Asterixis (flapping tremor of the hands) may be seen in stage II encephalopathy. Simple tasks, such as handwriting, become difficult. Inability to reproduce a simple figure is referred to as constructional apraxia.
• In early stages, patient's deep reflexes are hyperactive; with worsening encephalopathy, reflexes disappear, and extremities become flaccid.
• Occasionally fetor hepaticus, a characteristic breath odor like freshly mowed grass, acetone, or old wine, may be noticed.

• Electroencephalogram (EEG) shows generalized slowing, an increase in the amplitude of brain waves, and characteristic triphasic waves.
• Serum ammonia measurements are evaluated.
• Daily handwriting or drawing samples can be assessed if hepatic encephalopathy is suspected; constructional apraxia reveals progression.

• Lactulose (Cephulac) is given to reduce serum ammonia level. Patient should be observed for watery diarrheal stools, which indicate lactulose overdose, and monitored for hypokalemia and dehydration.
• IV glucose is given to minimize protein breakdown, and vitamins are given to correct deficiencies and electrolyte imbalances (especially potassium).
• Antibiotic agents are given if needed—such as Neomycin, metronidazole (Flagyl), and rifaximin (Xifaxan)—to reduce levels of ammonia-forming bacteria in the colon; no benefit has been shown for long-term treatment with these antibiotic drugs.
• Patients who are comatose or who have encephalopathy that is refractory to lactulose and antibiotic therapy should have their protein intake moderately restricted; enteral feeding is provided for patients whose encephalopathic state persists.
• Medications that may precipitate encephalopathy (e.g., sedative medications, tranquilizers, analgesic agents) should be discontinued.
• Benzodiazepine antagonists (flumazenil) can be given.

• Maintain a safe environment to prevent bleeding, injury, and infection.
• Administer the prescribed treatments and monitor the patient for the numerous potential complications.
• Assess neurologic and mental status.
• Record fluid input and output (I&O) and body weight daily and vital signs every 4 hours.
• Assess potential sites of infection (peritoneum, lungs); report abnormal findings promptly.
• Monitor serum ammonia level daily.
• Encourage deep breathing and position changes to prevent the development of atelectasis, pneumonia, and other respiratory complications.
• Communicate with the patient's family to inform them about the patient's status and support them by explaining the procedures and treatments that are part of the patient's care.
• Ask the family to observe patient for subtle signs of recurrent encephalopathy. Explain that rehabilitation after recovery is likely to be prolonged.
• Advise on caloric intake and protein intake: 35 to 40 kcal/kg body weight per day and 1.0 to 1.5 g/kg body weight per day.
• Educate patient about ways to administer lactulose and monitor for side effects.
• Refer patient for home care nurse visits to assess home environment to identify risk of falls and other injuries.
• Reinforce previous education and remind the patient and family about the importance of dietary restrictions, close monitoring, and follow-up.
• Assess patient's physical and mental status and compliance with prescribed therapeutic regimen.
• Refer to psychologists, psychiatric liaison nurses, case managers, social workers, spiritual advisor, or therapists to assist family members with coping. Provide support and education if alcohol played a role in the liver disease and refer to Alcoholics Anonymous or Al-Anon.

For more information, see Chapter 49 in Hinkle, J. L., & Cheever, K. H. (2018). Brunner and Suddarth's textbook of medical-surgical nursing (14th ed.). Philadelphia, PA: Lippincott Williams & Wilkins.