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John C. Lettsome noted in 1787 hyperesthesia and paralysis in legs more than arms of patients, a characteristic of alcoholic polyneuropathy. The first description of symptoms associated with alcoholic polyneuropathy were recorded by John C. Lettsome in 1787 when he noted hyperesthesia and paralysis in legs more than arms of patients. [2]
The management of lipodermatosclerosis may include treating venous insufficiency with leg elevation and elastic compression stockings. [9] In some difficult cases, the condition may be improved with the additional use of the fibrinolytic agent, stanozol. Fibrinolytic agents use an enzymatic action to help dissolve blood clots.
Person with cirrhosis and associated pain in the right upper region of the abdomen. Cirrhosis can take quite a long time to develop, and symptoms may be slow to emerge. [13] Some early symptoms include tiredness, weakness, loss of appetite, weight loss, and nausea. [13] Early signs may also include redness on the palms known as palmar erythema ...
Liver cirrhosis can develop in about 7% to 40% of treated patients. People with the highest risk for progression to cirrhosis are those with incomplete response to treatment, treatment failure, and multiple relapses. Once cirrhosis develops, management of liver cirrhosis in autoimmune hepatitis is standard regardless of etiology.
Zieve's syndrome is an acute metabolic condition that can occur during withdrawal from prolonged heavy alcohol use. It is defined by hemolytic anemia (with spur cells and acanthocytes), hyperlipoproteinemia (excessive blood lipoprotein), jaundice (elevation of unconjugated bilirubin), and abdominal pain. [1]
It is defined as an effusion of over 500 mL in people with liver cirrhosis that is not caused by heart, lung, or pleural disease. It is found in 5–10% of people with liver cirrhosis and 2–3% of people with pleural effusions. In cases of decompensated liver cirrhosis, prevalence rises significantly up to 90%. [1]
The exact definition of "rapid" is somewhat debatable, and different sub-divisions exist, which are based on the time from onset of first hepatic symptoms to onset of encephalopathy. One scheme defines "acute hepatic failure" as the development of encephalopathy within 26 weeks of the onset of any hepatic symptoms.
Positive symptoms include biliary colic, acute pancreatitis, obstructive jaundice and less commonly, liver enlargement and abnormal liver function tests. [1] Additional complications in the acute setting include ascending cholangitis , gallbladder empyema , clotting within the hepatic and portal veins , sepsis and death.