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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 .
[2] [6] It may be supported by blood ammonia levels, an electroencephalogram, or computer tomography (CT scan) of the brain. [4] [6] Hepatic encephalopathy is possibly reversible with treatment. [1] This typically involves supportive care and addressing the triggers of the event. [4] Lactulose is frequently used to decrease ammonia levels. [1]
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]
The syndrome is associated with changes on blood tests such as a high blood ammonia level, low blood sugar level, and prolonged prothrombin time. [2] Often, the liver is enlarged in those who have the syndrome. [2] Prevention is typically by avoiding the use of aspirin in children. [1]
The inability of the liver to metabolize ammonia to urea damages the brain cells. The cause is thought to be predominantly related to abnormal ammonia metabolism. [6] Other metabolic encephalopathies (often in conjuction with drowsiness or stupor), especially in decompensated cirrhosis or acute liver failure. Kidney failure and azotemia. Wilson ...
The compound volatile dimethyl sulfide has been associated with it, [3] raising the possibility of an objective noninvasive measure of liver failure. [ 4 ] [ 5 ] A secondary form of trimethylaminuria is also associated with liver failure, and it has been suggested that trimethylamine is also a contributor to the odor of fetor hepaticus.
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