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The diagnosis of hepatic encephalopathy is a clinical one, once other causes for confusion or coma have been excluded; no test fully diagnoses or excludes it. Serum ammonia levels are elevated in 90% of people, but not all hyperammonaemia (high ammonia levels in the blood) is associated with encephalopathy.
Hyperammonemia, or high ammonia levels, is a metabolic disturbance characterised by an excess of ammonia in the blood. Severe hyperammonemia is a dangerous condition that may lead to brain injury and death. It may be primary or secondary. Ammonia is a substance that contains nitrogen. It is a product of the catabolism of protein.
The presence of Alzheimer type II astrocytes is a key indicator of hepatic encephalopathy, and may be induced by increased bodily ammonia. [10] In hepatic encephalopathy, Alzheimer type II astrocytes are characterized by thin chromatin and increased glycogen levels. [5]
Ammonia is normally metabolized by the liver; as cirrhosis causes both decreased liver function and increased portosystemic shunting (allowing blood to bypass the liver), systemic ammonia levels gradually rise and lead to encephalopathy. [137] Most pharmaceutical approaches to treating hepatic encephalopathy focus on reducing ammonia levels. [138]
Lactulose is a non-absorbable sugar used in the treatment of constipation and hepatic encephalopathy. [3] [4] It is administered orally for constipation, and either orally or rectally for hepatic encephalopathy. [3] It generally begins working after 8–12 hours, but may take up to 2 days to improve constipation. [1] [2]
From November 1995 to November 1996 in France, a national survey of pediatric departments for children under 15 years of age with unexplained encephalopathy and a threefold (or greater) increase in serum aminotransferase and/or ammonia led to the identification of nine definite cases of Reye syndrome (0.79 cases per million children). Eight of ...
Menopause affects women’s health and well-being on both micro and macro levels. Women who hit menopause before 45 are at increased risk of cardiovascular problems and dying earlier than women ...
One scheme defines "acute hepatic failure" as the development of encephalopathy within 26 weeks of the onset of any hepatic symptoms. This is sub-divided into "fulminant hepatic failure", which requires onset of encephalopathy within 8 weeks, and "subfulminant", which describes onset of encephalopathy after 8 weeks but before 26 weeks. [6]