Abstract
Hepatic encephalopathy (HE) is a functional and generally reversible alteration of the central nervous system that appears in patients with acute and chronic liver disease. The pathogenesis of HE is not well understood (this aspect is deeply discussed in another chapter of this issue) although it has been suggested that the key mechanism is due to the inability of the liver to eliminate endogen and exogen products which are toxic to the brain. These substances reach the systemic blood stream because of the presence of hepatic failure, and the development of portosystemic shunts. Both mechanisms allow the intestinal blood to reach the brain without being cleared by the liver (1).
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Rodés, J. (1993). Clinical Manifestations and Therapy of Hepatic Encephalopathy. In: Grisolía, S., Felipo, V. (eds) Cirrhosis, Hyperammonemia, and Hepatic Encephalopathy. Advances in Experimental Medicine and Biology, vol 341. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-2484-7_4
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DOI: https://doi.org/10.1007/978-1-4615-2484-7_4
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