Hepatic encephalopathy (also called hepatic coma or por-tosystemic encephalopathy) is a complex neuropsychiatric syn-drome that may complicate advanced liver disease and/or ex-tensive portosystemic collateral formation (shunting). Two major forms of hepatic encephalopathy are recognized: acute and chronic.

Acute hepatic encephalopathy usually occurs in the setting of fulminant hepatic failure. Cerebral edema plays a more im-portant role in this setting: coma is common and mortality is extremely high. Chronic hepatic encephalopathy usually occurs with chronic liver disease, commonly manifests as subtle dis-turbances of neurologic function, and is often reversible.

The pathogenesis of hepatic encephalopathy is thought to involve the inadequate hepatic removal of predominantly ni-trogenous compounds or other toxins ingested or formed in the gastrointestinal tract. Inadequate hepatic removal results from impaired hepatocyte {unction, as well as the extensive shunting of splanchnic blood directly into the systemic circulation by portosystemic collateral vessels. Nitrogenous and other ab-sorbed compounds are thought to gain access to the central ner-vous system and to lead to disturbances in neuronal function. mmonia, derived from both amino acid deamination and bac-terial hydrolysis of nitrogenous compounds in the gut, has been trongly implicated in the pathogenesis of hepatic en-cephalopathy, but its blood levels correlate poorly with the resence or degree of encephalopathy. In vestigators have sug-gested that ammonia generated in the stomach (especially in the presence of hypochloridia) by Helicobacter pylorimay con-tribute to the development of encephalopathy. Other proposed neurotoxins include y-aminobutyric acid, mercaptans, short-chain fatty acids, and benzodiazepine-like compounds. Mer-captans are also thought to produce the characteristic breath odor (fetor hepaticus) of patients with chronic liver failure. Another hypothesis suggests that an imbalance between plasma branched-chain and aromatic amino acids, a common conse-quence of severe liver disease, lead to decreased synthesis of normal neurotransmitters and to increased formation of "false neurotransmitters" from aromatic amino acids in the central nervous system. In addition, altered cerebral metabolism (dis-turbed Na+_K+_ATPase activity), zinc deficiency causing de-creased activity of urea-cycle enzymes, and deposition of man-ganese in the basal ganglia have been implicated as possible mechanisms.

The clinical features of hepatic encephalopathy include disturbances of higher neurologic function E intellectual and personality disorders, dementia, inability to copy simple dia-grams (constructional apraxia), disturbance of consciousness], disturbances of neuromuscular function (asterixis, hyperreflex- ia, myoclonus), and rarely, a Parkinson-like syndrome and progressive, paraplegia. As with other metabolic en-cephalopathies, which may show many of the signs of hepatic encephalopathy, asymmetric neurologic findings are unusual but ca'n occur, and brain stem reflexes (pupillary light, oculovestibular, and oculocephalic responses) are preserved un-til extremely late in the course of the disease. Hepatic en-cephalopathy is usually divided into stages according to its severity. Subtle disorders of psychomotor function may exist in as many as 50 % to 70 % of patients with cirrhosis in whom a conventional neurologic examination is normal. Such subclini-cal encephalopathy (termed stage 0 encephalopathy) is impor-tant in that it may impair work performance. One of the earli-est manifestations is the alteration of the patient's normal sleep-wake cycle. The differential diagnosis of hepatic en-cephalopathy includes hypoglycemia, subdural hematoma, meningitis, and sedative drug overdose, all of which are com-mon in patients with liver disease, particularly patients with alcoholism.

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