Hepatic encephalopathy is a neuropsychiatric syndrome consisting of altered neurological function associated with acute or chronic liver disease and portal systemic shunting. Exclusion of other disorders of the central nervous system (CNS) is important to establish the diagnosis. The development of hepatic encephalopathy in a cirrhotic patient indicates decompensation of a previously stable liver disease, or more frequently, it represents the effect of a transient precipitating factor. Hepatic encephalopathy generally implies a poor prognosis; its severity is a key component of the Child-Pugh score, an important prognostic system in chronic liver disease. In contrast, onset of hepatic encephalopathy in patients with acute liver failure (ALF), defines a fulminant course and is associated with risk of life threatening complications, including cerebral edema and intracranial hypertension.
In spite of the common occurrence of hepatic encephalo-pathy in patients with cirrhosis, there is no reliable laboratory method to recognize and objectively assess its severity. Recently,the final report ofa working party in 1998 (Ferenci et al, 2002)proposed a new classification for hepatic encephalopathy. From a clinical presentation and course standpoints, hepatic encephalopathy can be episodic, persistent, or minimal. Most episodes of encephalopathy can be traced to precipitating factors, but some can be spontaneous and recurrent as observed in patients with decompensated cirrhosis. Minimal encephalopathy has substituted the previous term of subclinical hepatic encephalopathy. These patients appear clinically nonencephalopathic yet exhibit subtle cognitive deficits on neuropsychological testing. The clinical relevance and therapy of minimal encephalopathy is under investigation.
In the context of this revised conceptual framework, we review here the current approaches to diagnosis and management of hepatic encephalopathy.
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