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A.D.A.M. Medical Encyclopedia [Internet]. Atlanta (GA): A.D.A.M.; 2013.

A.D.A.M. Medical Encyclopedia.

Hepatic encephalopathy

Hepatic coma; Encephalopathy - hepatic

Last reviewed: October 16, 2011.

Hepatic encephalopathy is a worsening of brain function that occurs when the liver is no longer able to remove toxic substances in the blood.

Causes, incidence, and risk factors

Hepatic encephalopathy is caused by disorders that affect the liver. These include disorders that reduce liver function (such as cirrhosis or hepatitis) and conditions in which blood circulation does not enter the liver. The exact cause of hepatic encephalopathy is unknown.

An important job of the liver is to change toxic substances that are either made by the body or taken into the body (such as medicines) and make them harmless. However, when the liver is damaged, these "poisons" may build up in the bloodstream.

Ammonia, which is produced by the body when proteins are digested, is one of the harmful substances that is normally made harmless by the liver. Many other substances may also build up in the body if the liver is not working well. They can cause damage to the nervous system.

Hepatic encephalopathy may occur suddenly in people who previously had no liver problems when damage occurs to the liver. More often, the condition is seen in people with chronic liver disease.

Hepatic encephalopathy may be triggered by:

  • Eating too much protein
  • Electrolyte abnormalities (especially a decrease in potassium) from vomiting, or from treatments such as paracentesis or taking diuretics ("water pills")
  • Bleeding from the intestines, stomach, or esophagus
  • Infections
  • Kidney problems
  • Low oxygen levels in the body
  • Shunt placement or complications (See: Transjugular intrahepatic portosystemic shunt )
  • Surgery
  • Use of medications that suppress the central nervous system (such as barbiturates or benzodiazepine tranquilizers)

Disorders that can mimic or mask symptoms of hepatic encephalopathy include:

Hepatic encephalopathy may occur as an acute, potentially reversible disorder. Or it may occur as a chronic, progressive disorder that is associated with chronic liver disease.

Symptoms

Symptoms many begin slowly and gradually worsen, or they may begin suddenly and be severe from the start.

Symptoms may be mild at first. Family members or caregivers may notice that the patient has:

  • Breath with a musty or sweet odor
  • Change in sleep patterns
  • Changes in thinking
  • Confusion that is mild
  • Forgetfulness
  • Mental fogginess
  • Personality or mood changes
  • Poor concentration
  • Poor judgment
  • Worsening of handwriting or loss of other small hand movements

More severe symptoms may include:

  • Abnormal movements or shaking of hands or arms
  • Agitation, excitement, or seizures (occur rarely)
  • Disorientation
  • Drowsiness or confusion
  • Inappropriate behavior or severe personality changes
  • Slurred speech
  • Slowed or sluggish movement

Patients with hepatic encephalopathy can become unconscious, unresponsive, and possibly enter a coma.

Patients with hepatic encephalopathy are often not able to care for themselves because of these symptoms.

Signs and tests

Nervous system signs may change. Signs include:

  • Coarse, "flapping" shaking of the hands when attempting to hold the arms out in front of the body and lift the hands
  • Abnormal mental status, particularly cognitive (thinking) tasks such as connecting numbers with lines
  • Signs of liver disease, such as yellow skin and eyes (jaundice) and fluid collection in the abdomen (ascites), and occasionally a musty odor to the breath and urine

Tests may include:

Treatment

Hepatic encephalopathy may become a medical emergency. Hospitalization is required.

The first step is to identify and treat any factors that may have caused hepatic encephalopathy.

Gastrointestinal bleeding must be stopped. The intestines must be emptied of blood. Infections, kidney failure, and electrolyte abnormalities (especially potassium) need to be treated.

Life support may be necessary to help with breathing or blood circulation, particularly if the person is in a coma. The brain may swell, which can be life-threatening.

Patients with severe, repeated cases of encephalopathy may be told to reduce protein in the diet to lower ammonia production. However, dietary counseling is important, because too little protein in the diet may cause malnutrition. Critically ill patients may need specially formulated intravenous or tube feedings.

Lactulose may be given to prevent intestinal bacteria from creating ammonia, and as a laxative to remove blood from the intestines. Neomycin may also be used to reduce ammonia production by intestinal bacteria. Rifaximin, a new antibiotic, is also effective in hepatic encephalopathy.

Sedatives, tranquilizers, and any other medications that are broken down by the liver should be avoided if possible. Medications containing ammonium (including certain antacids) should also be avoided. Other medications and treatments may be recommended. They may have varying results.

Expectations (prognosis)

Acute hepatic encephalopathy may be treatable. Chronic forms of the disorder often keep getting worse or continue to come back.

Both forms may result in irreversible coma and death. Approximately 80% (8 out of 10 patients) die if they go into a coma. Recovery and the risk of the condition returning vary from patient to patient.

Complications

Calling your health care provider

Call your health care provider if any change in mental state or other nervous system problem occurs, particularly if there is a known or suspected liver disorder. Hepatic encephalopathy can rapidly get worse and become an emergency condition.

Prevention

Treating liver disorders may prevent some cases of hepatic encephalopathy. Avoiding heavy drinking and intravenous drug use can prevent many liver disorders.

If there are any nervous system symptoms in a person with known or suspected liver disease, call for immediate medical attention.

References

  1. Garcia-Tsao G. Cirrhosis and its sequelae. In: Goldman L, Ausiello D, eds. Cecil Medicine. 24th ed. Philadelphia, Pa: Saunders Elsevier; 2011:chap 156.

Review Date: 10/16/2011.

Reviewed by: George F. Longstreth, MD, Department of Gastroenterology, Kaiser Permanente Medical Care Program, San Francisco, CA. Also reviewed by David Zieve, MD, MHA, Medical Director, A.D.A.M., Inc.

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The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition. A licensed medical professional should be consulted for diagnosis and treatment of any and all medical conditions. Call 911 for all medical emergencies. Links to other sites are provided for information only — they do not constitute endorsementscof those other sites. © 1997–2011 A.D.A.M., Inc. Any duplication or distribution of the information contained herein is strictly prohibited.

Copyright © 2013, A.D.A.M., Inc.

A.D.A.M., Inc. is accredited by URAC, also known as the American Accreditation HealthCare Commission (www.urac.org). URAC's accreditation program is an independent audit to verify that A.D.A.M. follows rigorous standards of quality and accountability. A.D.A.M. is among the first to achieve this important distinction for online health information and services. Learn more about A.D.A.M.'s editorial policy, editorial process and privacy policy. A.D.A.M. is also a founding member of Hi-Ethics and subscribes to the principles of the Health on the Net Foundation (www.hon.ch).

The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition. A licensed medical professional should be consulted for diagnosis and treatment of any and all medical conditions. Call 911 for all medical emergencies. Links to other sites are provided for information only — they do not constitute endorsementscof those other sites. © 1997–2011 A.D.A.M., Inc. Any duplication or distribution of the information contained herein is strictly prohibited.

Copyright © 2013, A.D.A.M., Inc.

What works?

  • Nutritional support for patients with liver disease
    Patients with liver diseases, especially decompensated cirrhosis, commonly have weight loss and muscle wasting. It is known that such patients have poorer clinical outcomes than patients with similar diagnoses but without such weight loss or muscle wasting. If the problem is just deprivation of nutrients, it would be expected that the provision of some type of nutrition should result in better outcomes. Nutrients in addition to food, or in place of food when food is not taken in sufficient amounts, can be provided in a manner whereby the patient voluntarily consumes them by drinking various nutrient formulations. Nutrients can also be provided in an involuntary manner; tubes can be placed in the vein (parenteral nutrition) or intestinal tract (enteral nutrition) and nutrient solutions infused through them. All of these nutritional interventions have associated economic costs and also can produce a variety of complications (including vomiting, diarrhoea, and altered metabolic functions (for example, high blood sugar)). Thus, it is important to determine if such nutritional interventions (that is, the provision of nutrients in some manner other than just as food) do result in improvements in clinical outcomes. Since the best way to make such a determination is to undertake randomised trials, in which patients are assigned by chance to receive, or not receive, one or another of these treatments, this systematic review was undertaken to identify and summarise this information. Randomised trials comparing patients with liver diseases who were assigned to receive parenteral nutrition, enteral nutrition, or oral nutritional supplements to similar patients assigned not to receive any nutritional intervention were collected. The three nutritional interventions were considered separately. In addition, within each category of nutritional intervention, patients with medical conditions were compared separately from patients with surgical conditions. Thus there were six primary analyses, medical patients receiving or not receiving parenteral nutrition, surgical patients receiving or not receiving parenteral nutrition, medical patients receiving or not receiving enteral nutrition, surgical patients receiving or not receiving enteral nutrition, medical patients receiving or not receiving supplements by mouth, and surgical patients receiving or not receiving supplements by mouth. The outcomes of interest were mortality, hepatic morbidity (ascites, gastrointestinal bleeding, encephalopathy), quality of life, adverse events, infections, cost, duration of hospitalisation, jaundice, postoperative complications (only for the surgical trials), and nutritional outcomes (for example, body weight). A total of 37 randomised trials were identified. All but one had a high risk of systematic error (bias, that is overestimation of benefits and underestimation of harms). When the data were combined, most of the analyses failed to demonstrate a difference. There were some significant differences observed. These were that 1) parenteral nutrition reduced serum bilirubin more rapidly and improved one type of nutritional outcome (nitrogen balance) in medical patients with jaundice, and may have reduced some postoperative complications; 2) enteral nutrition may have improved nitrogen balance in medical patients, and reduced postoperative complications in surgical patients; and 3) supplements reduced the occurrence of ascites and also may have decreased the number of infections. Furthermore, the receipt of supplements (especially ones containing branched‐chain amino acids) may have been helpful in the treatment of patients with hepatic encephalopathy. No significant effects were seen from the use of supplements in surgical patients. None of these observed benefits can be said to be definitively present because of the presence of methodologic flaws in the trials, which may have produced an overestimation of the observed effect. Moreover, due to too few patients included in the trials with two few outcome measures, both spurious significant findings and spurious insignificant findings cannot be excluded. The data are not strong enough to justify a recommendation to use these nutritional interventions routinely. We need well‐designed and well‐conducted randomised trials to prove that such therapy is indeed efficacious.
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