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This is a treatment for hepatic encephalopathy. [15] Treatment of severe hyperammonemia (serum ammonia levels greater than 1000 μmol/L) should begin with hemodialysis if it is otherwise medically appropriate and tolerated. [12]
[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]
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. [139] Most pharmaceutical approaches to treating hepatic encephalopathy focus on reducing ammonia levels. [140]
A metabolic encephalopathy develops, and this can progress to coma and death without treatment. [4] Ammonia is only toxic to the brain, other tissues can handle elevated ammonia concentrations without problems. [5] Later onset forms of OTC deficiency can have variable presentations.
Ammonia scavengers and arginine may be prescribed to better manage ammonia levels. Patients with brain edema caused by hepatic encephalopathy should avoid glycerol infusions because glycerol is metabolized in the liver to generate NADH, which worsens the condition and may be fatal.
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.
The complications are hepatic encephalopathy and impaired protein synthesis (as measured by the levels of serum albumin and the prothrombin time in the blood). The 1993 classification defines hyperacute as within 1 week, acute as 8–28 days, and subacute as 4–12 weeks; [ 1 ] both the speed with which the disease develops and the underlying ...