Hepatic Encephalopathy



Hepatic encephalopathy (also called hepatic coma or portosystemic encephalopathy) is a com­plex neuropsychiatric syndrome that may com­plicate advanced liver disease and/or extensive portosystemic collateral formation (shunting). Two major forms of hepatic encephalopathy are recognized:

Acute hepatic encephalopathy usually occurs in the setting of fulminant hepatic failure. Cere­bral edema plays a more important role in this setting: coma is common and mortality is very high .

Chronic hepatic encephalopathy usually oc­curs with chronic liver disease, commonly man­ifests as subtle disturbances of neurological func­tion, and is often reversible.

The pathogenesis of hepatic encephalopathy is unknown but is thought to involve the inadequate hepatic removal of predominantly nitrogenous compounds or other toxins ingested or formed in the gastrointestinal tract. Inadequate hepatic re­moval results from impaired hepatocyte function as well as the extensive shunting of splanchnic blood directly into the systemic circulation via portosystemic collaterals. Nitrogenous and other absorbed compounds are thought to gain access to the central nervous system, leading to disturb­ances in neuronal function. Ammonia, derived from both amino acid deamination and bacterial hydrolysis of nitrogenous compounds in the gut, has been strongly implicated in the pathogenesis of hepatic encephalopathy. However, blood levels of ammonia correlate poorly with the presence or degree of encephalopathy. Other proposed neu­rotoxins include gamma-aminobutyric acid, mercaptans, and short chain fatty acids. Mercaptans 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 con­sequence of severe liver disease, leads to de­creased synthesis of normal neurotransmitters and to increased formation of “false neurotrans­mitters” from aromatic amino acids in the central nervous system.
The clinical features of hepatic encephalopathy include disturbances of higher neurological func­tion (intellectual and personality disorders, de­mentia, inability to copy simple diagrams [i.e., constructional apraxia], disturbance of conscious­ness), disturbances of neuromuscular function (asterixis, hyperreflexia, myoclonus), and rarely, a Parkinson-like syndrome and progressive par­aplegia. As with other metabolic encephalopa­thies (which may show many of the signs of he­patic encephalopathy) asymmetrical neurological findings are unusual but can occur, and brain stem reflexes (e.g., pupillary light, oculovestibular, and oculocephalic responses) are preserved until very late. Hepatic encephalopathy is usually divided into stages according to its severity . Subtle disorders of psychomotor function may exist in many patients with cirrhosis in whom conventional neurological examination is normal. Such subclinical encephalopathy (termed stage 0 encephalopathy) is of importance in that it may impair work performance.
The differential diagnosis of hepatic encepha­lopathy includes hypoglycemia, subdural hema­toma, meningitis, and sedative drug overdosage, all of which are common in patients, particularly alcoholics, with liver disease.





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