Hepatic encephalopathy: clinical features
Written and reviewed by Dr Ibrahim Imam, Consultant Neurologist. Last reviewed .
Hepatic encephalopathy: clinical features. It results from high ammonia due to porto-systemic shunting. Fully referenced neurology checklist.
Pathogenesis
- It results from high ammonia due to porto-systemic shunting
- The ammonia is metabolized to glutamine in brain cells
- Glutamine increases cellular osmotic pressure
- Ammonia also leads to raised extracellular GABA
Triggers
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Types
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Clinical features
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Severity scales
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Differential diagnosis
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References
- Suraweera D, Sundaram V, Saab S. Evaluation and management of hepatic encephalopathy: current status and future directions. Gut Liver 2016; 10:509-519.
- Ellul MA, Gholkar SA, Cross TJ. Hepatic encephalopathy due to liver cirrhosis. BMJ 2015; 351:h4187.
- Savlan I, Liakina V, Valantinas J. Concise review of current concepts on nomenclature and pathophysiology of hepatic encephalopathy. Medicina (Kaunas) 2014; 50:75-81.
- Ferenci P, Lockwood A, Mullen K, et al. Hepatic encephalopathy-definition, nomenclature, diagnosis, and quantification: final report of the working party at the 11th World Congresses of Gastroenterology, Vienna, 1988. Hepatology 2002; 35:716-721.
- Weissenborn K, Enne JC, Schomerus H, et al. Neuropsychological characterization of hepatic encephalopathy. J Hepatol 2001; 34:768-773.
