Medical Clinic

Hepatic Encephalopathy

Hepatic encephalopathy (also called hepatic coma, portal-systemic encephalopathy) is a neurologic syndrome that develops as a complication of aggressive fulminant hepatitis or chronic hepatic disease. This syndrome is most common in patients with cirrhosis. It may be acute and self-limiting or chronic and progressive. In advanced stages, the prognosis is extremely poor despite vigorous treatment.


Hepatic encephalopathy is caused by disorders affecting the liver. These include disorders that reduce liver function and conditions where blood circulation bypasses the liver.

However, when the liver cannot properly metabolize and detoxify substances in the body, toxic substances build up in the bloodstream. One substance believed to be particularly toxic to the central nervous system is ammonia, which is produced by the body when proteins are digested, but is normally detoxified by the liver. Many other substances may also accumulate in the body and contribute to damage to the nervous system.

In people with otherwise stable liver disorders, hepatic encephalopathy may be triggered by episodes of gastrointestinal bleeding, excessive intake of dietary protein, electrolyte abnormalities, infections, renal disease, and procedures that shunt blood past the liver.

Signs and Symptoms

Clinical features vary, depending on the severity of neurologic involvement. The disorder usually progresses through four stages, but the patient's symptoms can fluctuate from one stage to another.

In the prodromal stage, early symptoms are typically overlooked because they're so subtle. The patient's history obtained from the patient or from a family member or caregiver may reveal slight personality changes, such as agitation, belligerence, disorientation, and forgetfulness. The patient may also have trouble concentrating or thinking clearly. He may report feeling fatigued or drowsy. He may have slurred or slowed speech. On inspection, you may observe a slight tremor.

In the impending stage, the patient undergoes continuing mental changes. He may be confused and disoriented as to time, place, and person. Inspection continues to reveal tremors that have progressed to asterixis (also called liver flap and flapping tremor). Asterixis - the hallmark of hepatic encephalopathy­refers to quick, irregular extensions and flexions of the wrists and fingers, when the wrists are held out straight and the hands flexed upward. On inspection, you may observe lethargy and aberrant behavior. Some patients demonstrate apraxia. When asked, the patient is unable to reproduce a simple design such as a star.

In the stuporous stage, the patient shows marked mental confusion. On inspection, he appears drowsy and stuporous. Yet he can still be aroused and is often noisy and abusive. Hyperventilation, muscle twitching, and asterixis are also evident.

In the comatose stage, the patient can't be aroused and is obtunded with no asterixis. Seizures, though uncommon, may occur. Palpation may reveal hyperactive reflexes and a positive Babinski's sign. The patient often has fetor hepaticus (musty odor of the breath and urine). Fetor hepaticus may occur in other stages also. Eventually this stage progresses to coma; it's usually fatal.

Diagnostic tests

Serum ammonia levels in venous and arterial samples are elevated and, together with characteristic clinical features, highly suggest hepatic encephalopathy.

An EEG shows slowing waves as the disease progresses.


The goal of therapy is to eliminate the underlying cause of the disorder and to lower serum ammonia levels to stop progression of encephalopathy. In mild cases, treating the underlying cause of encephalopathy may reverse the symptoms. In most patients, the toxic products, often ammonia, must also be eliminated from the body.

Treatments to eliminate ammonia from the GI tract include sorbitol-induced catharsis to produce osmotic diarrhea, continuous aspiration of blood from the stomach, reduction of dietary protein intake, and administration of lactulose to reduce serum ammonia levels.

Lactulose traps ammonia in the bowel and promotes its excretion. It's effective because bacterial enzymes change lactulose to lactic acid, thereby rendering the colon too acidic for bacterial growth. At the same time, the resulting increase in free hydrogen ions prevents diffusion of ammonia through the mucosa; lactulose promotes conversion of systemically absorbable ammonia to ammonium, which is poorly absorbed and can be excreted. Lactulose syrup may be given orally. In acute hepatic coma, lactulose may be administered by retention enema. Lactulose therapy requires careful monitoring of fluid and electrolyte balance.

Although it's now considered a second-line treatment because of potential toxicity, neomycin may be given to suppress bacterial flora (preventing them from converting amino acids into ammonia). Neomycin is administered orally or by retention enema. Although neomycin is nonabsorbable at recommended dosages of 3 to 4 g/day, an amount that exceeds 4 g/day may produce irreversible hearing loss and nephrotoxicity.

Treatment may also include potassium supplements (80 to 120 mEq/day given by mouth or I.V.) to correct alkalosis (from increased ammonia levels), especially if the patient is taking diuretics. Salt-poor albumin may be used to maintain fluid and electrolyte balance, replace depleted albumin levels, and restore plasma.

Other treatments that have been tried, usually with little success, are hemodialysis and exchange transfusions.


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 neurologic symptoms in a person with known or suspected liver disease, call for immediate medical attention.

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