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  • Diagnosis can often be made during physical examination by checking for fetor hepaticus and asterixis, and evaluating mental status using serial 7's and the "A" deletion test.
  • Precipitating factors include gastrointestinal bleeding, sepsis, azotemia, sedative or analgesic use, and noncompliance with medications.
  • Consider other causes (eg, infections, intracranial bleeding, metabolic abnormalities), in patients with known cirrhosis and prior evidence of portal system encephalopathy who present with altered mental status.
  • Mental changes in patients with subclinical or minimal hepatic encephalopathy can impair automobile handling skills; patients and their families should be advised of this risk.

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Hepatic encephalopathy, also referred to as portal systemic encephalopathy (PSE), is a complex neuropsychiatric disorder resulting from chronic parenchymal liver disease with liver cell failure, often in conjunction with portal systemic shunts, either naturally occurring or surgically created. However, PSE can occur in individual with normal liver tests or with large spontaneous or surgically created shunts. PSE is characterized by changes in personality, level of consciousness, motor function, and cognition. Changes in cognition may be quite subtle, as pointed out below.

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Hepatic encephalopathy can be characterized as being episodic or chronic resistant. The episodic form may be spontaneous, precipitated, or recurrent; in the chronic resistant form, patients have persistent mild stage 1–2 or severe stage 2–4 disease. Patients can have minimal or subclinical encephalopathy with no obvious abnormalities in cognition, personality, or behavior but with abnormal psychometric tests. Patients with advanced chronic liver disease and longstanding portal systemic shunting may also develop evidence of non-Wilsonian hepatolenticular degeneration.

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Table 44–1 summarizes putative toxins that have been implicated in the pathogenesis of hepatic encephalopathy. Although the precise pathogenesis of hepatic encephalopathy is unknown, accumulation of nitrogenous products derived from the gut can have adverse effects on brain function and is believed to play a major role.

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Table 44–1. Putative Toxins Causing Hepatic Encephalopathy.

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