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[Hepatic encephalopathy].

Philip Hilgard1, Guido Gerken

  • 1Klinik für Gastroenterologie und Hepatologie, Zentrum für Innere Medizin, Universitätsklinikum Essen, Hufelandstrasse 55, 45122 Essen, Germany.

Medizinische Klinik (Munich, Germany : 1983)
|October 19, 2004
PubMed
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Hepatic encephalopathy (HE) involves psychomotor symptoms due to impaired liver detoxification, with ammonia playing a key role. Treatment focuses on circulation, toxin reduction, and liver transplantation for severe cases.

Area of Science:

  • Hepatology
  • Neurology
  • Gastroenterology

Background:

  • Hepatic encephalopathy (HE) presents with psychomotor symptoms in acute or chronic liver failure.
  • HE can also occur with portocaval shunting, independent of liver disease.
  • Impaired hepatic detoxification due to reduced hepatocytes or shunting allows toxin buildup.

Purpose of the Study:

  • To review current pathogenetic hypotheses of hepatic encephalopathy.
  • To discuss the classification and diagnosis of HE.
  • To outline therapeutic strategies for HE.

Main Methods:

  • Review of existing literature on hepatic encephalopathy pathogenesis.
  • Clinical classification based on West Haven criteria.
  • Discussion of diagnostic approaches and differential diagnoses.

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Main Results:

  • Ammonia is a central factor in HE pathogenesis, though its exact cerebral effects require further study.
  • HE is classified into acute and chronic forms, with chronic HE presenting as persistent or episodic.
  • Precipitating factors for episodic HE include diet, infection, and gastrointestinal bleeding.

Conclusions:

  • Liver transplantation is the only causal treatment for HE in liver failure.
  • Symptomatic treatment aims to stabilize circulation, remove toxins like ammonia, and manage precipitating factors.
  • Prophylaxis and therapy for brain edema are crucial in acute HE.