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Hepatic encephalopathy type B may arise in those who have undergone a TIPS procedure; in most cases this resolves spontaneously or with the medical treatments discussed below, but in a small proportion of about 5%, occlusion of the shunt is required to address the symptoms. [10] In hepatic encephalopathy type C, the identification and treatment ...
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. [24]
Subacute combined degeneration of spinal cord, also known as myelosis funiculus, or funicular myelosis, [1] also Lichtheim's disease, [2] [3] and Putnam-Dana syndrome, [4] refers to degeneration of the posterior and lateral columns of the spinal cord as a result of vitamin B 12 deficiency (most common).
Signs and symptoms of alcoholic hepatitis include jaundice (yellowing of the skin and eyes), ascites (fluid accumulation in the abdominal cavity), fatigue and hepatic encephalopathy (brain dysfunction due to liver failure). [3] Mild cases are self-limiting, but severe cases have a high risk of death.
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]
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.
Ischemic hepatitis, also known as shock liver, is a condition defined as an acute liver injury caused by insufficient blood flow (and consequently insufficient oxygen delivery) to the liver. [5] The decreased blood flow ( perfusion ) to the liver is usually due to shock or low blood pressure.
The serious symptoms of Reye syndrome appear to result from damage to cellular mitochondria, [14] at least in the liver, and there are a number of ways that aspirin could cause or exacerbate mitochondrial damage. A potential increased risk of developing Reye syndrome is one of the main reasons that aspirin has not been recommended for use in ...