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DOI: 10.1055/a-2647-5748
Hepatische Enzephalopathie bei Leberzirrhose
Hepatic encephalopathy in liver cirrhosisAuthors
Die hepatische Enzephalopathie (HE) ist eine häufige Komplikation der Leberzirrhose mit signifikanter Morbidität und Mortalität. Eine frühzeitige Erkennung und individualisierte Therapie der HE sind entscheidend, um Lebensqualität, Prognose und Alltagsfunktion der Patient*innen mit Leberzirrhose zu verbessern. Dieser Beitrag gibt einen Überblick über praxisnahe Diagnose- und Management-Strategien der HE bei Patient*innen mit Leberzirrhose.
Abstract
Hepatic encephalopathy (HE) is a common and serious complication of liver cirrhosis, associated with significant morbidity and mortality. Pathophysiologically, it results from a complex interplay of hyperammonemia, systemic inflammation, neuroinflammatory processes, and microbial dysbiosis. Clinically, HE ranges from subtle cognitive impairments (minimal HE) to coma (grade 4 HE). Diagnosis requires thorough clinical assessment and the use of specialized testing methods, particularly to detect subclinical alterations. In everyday practice, ammonia levels have limited diagnostic value but may be useful for differential diagnosis. The acute treatment of overt hepatic encephalopathy (OHE) is primarily based on the administration of lactulose, optionally supplemented with intravenous L-ornithine-L-aspartate. For secondary prophylaxis lactulose is the treatment of choice and in patients with recurrent episodes, the combination of rifaximin and lactulose is well established. Nutritional recommendations are a key component of therapy, especially to prevent sarcopenia. In cases of refractory HE or recurrent relapses despite guideline-based treatment, liver transplantation should always be considered. In general, early detection and individualized management of HE is essential to preserve and improve quality of life, prognosis, and functional independence of the affected patients.
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Die hepatische Enzephalopathie (HE) ist eine häufige Komplikation der Leberzirrhose und wird im Alltag oft übersehen.
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Die Pathophysiologie ist komplex und fußt auf einem Zusammenspiel aus Hyperammonämie, systemischer Inflammation, neuroinflammatorischen Prozessen und mikrobieller Dysbiose.
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Die HE wird anhand der West-Haven-Klassifikation eingeteilt.
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Die Akuttherapie der overten HE (OHE) basiert auf der Gabe von Laktulose, ggf. ergänzt durch L-Ornithin-L-Aspartat.
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Eine Sekundärprophylaxe sollte mit Laktulose durchgeführt werden. Nach einem Durchbruch-Rezidiv sollte Rifaximin ergänzt werden.
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Eine suffiziente Ernährung (mit ausreichender Protein-Zufuhr) ist die Basis der Primär- und Sekundärprophylaxe.
Publication History
Article published online:
09 February 2026
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