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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. It may be primary or secondary. Ammonia is a substance that contains nitrogen. It is a product of the catabolism of protein.
The underlying mechanism is believed to involve the buildup of ammonia in the blood, a substance that is normally removed by the liver. [2] The diagnosis is typically based on symptoms after ruling out other potential causes. [2] [6] It may be supported by blood ammonia levels, an electroencephalogram, or computer tomography (CT scan) of the ...
Dimethyl sulfide. Fetor hepaticus or foetor hepaticus (Latin, "liver stench" ("fetid liver") [1] (see spelling differences), also known as breath of the dead or hepatic foetor, is a condition seen in portal hypertension where portosystemic shunting allows thiols to pass directly into the lungs.
Treatment generally includes supportive care including pain management and possibly diuretics. [5] In those with severe disease due to a bone marrow transplant, defibrotide is a proposed treatment. [6] It has been approved for use in severe cases in Europe and the United States. [7] [8] A placebo controlled trial, however, has not been done as ...
In ALF, hepatic encephalopathy leads to cerebral edema, coma, brain herniation, and eventually death. Detection of encephalopathy is central to the diagnosis of ALF. It may vary from subtle deficit in higher brain function (e.g. mood, concentration in grade I) to deep coma (grade IV). Patients presenting as acute and hyperacute liver failure ...
Cirrhosis, also known as liver cirrhosis or hepatic cirrhosis, chronic liver failure or chronic hepatic failure and end-stage liver disease, is an acute condition of the liver in which the normal functioning tissue, or parenchyma, is replaced with scar tissue and regenerative nodules as a result of chronic liver disease.
Documented cases of Reye syndrome in adults are rare. The recovery of adults with the syndrome is generally complete, with liver and brain function returning to normal within two weeks of onset. [citation needed] In children, mild to moderate to severe permanent brain damage is possible, especially in infants.
Protein toxicity is the effect of the buildup of protein metabolic waste compounds, like urea, uric acid, ammonia, and creatinine.Protein toxicity has many causes, including urea cycle disorders, genetic mutations, excessive protein intake, and insufficient kidney function, such as chronic kidney disease and acute kidney injury.