Hepatic encephalopathy: clinical features
Evidence-based neurology checklist on hepatic encephalopathy: clinical features: 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…
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
Types
Clinical features
Severity scales
Differential diagnosis
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.
